Brain, Behavior, and Immunity最新文献

{"title":"The role of social support on change in C-reactive Protein and BMI among youth with and without child maltreatment history","authors":"Savannah A. Girod ,&nbsp;Aishwarya Ganguli ,&nbsp;Yo Jackson ,&nbsp;Christine Heim ,&nbsp;Idan Shalev ,&nbsp;Eric Claus ,&nbsp;Zachary Fisher ,&nbsp;Jennie Noll ,&nbsp;Chad Shenk ,&nbsp;Hannah M.C. Schreier","doi":"10.1016/j.bbi.2025.106250","DOIUrl":"10.1016/j.bbi.2025.106250","url":null,"abstract":"<div><div>Child maltreatment (CM) has long-term consequences for metabolic and inflammatory processes, but it is unclear when these associations emerge and whether other psychosocial resources (e.g., social support), can moderate these associations. This study examined (1) the extent to which a history of CM investigation was associated with changes in youth high-sensitivity C-reactive protein (hs-CRP) and body mass index (BMI) across a two-year period, and (2) the moderating role of social support from different sources (caregivers, siblings, and peers) on this association. Participants included 318 youth (ages 8–13, 49.7 % female, 72 % white, 82.7 % with past CM investigation) who completed baseline (Time 1) and two-year follow up (Time 2) visits. CM history, hs-CRP and BMI were assessed at T1. Caregiver, peer, and sibling support, hs-CRP, and BMI were assessed at T2. Adjusting for youth age, sex, race/ethnicity, household income, and hs-CRP and BMI at Time 1, no main effects of CM history on Time 2 hs-CRP or BMI were found (<em>p</em>s &gt; 0.28). However, independent of CM history, greater peer support was associated with lower BMI at Time 2 (β = -0.10, <em>p</em> = 0.005). Peer support further moderated the association between CM history and Time 2 BMI (β = -0.16, <em>p</em> = 0.007), such that CM history was associated with higher BMI only when peer support was relatively lower. Additionally, independent of CM history, greater sibling support was associated with lower hs-CRP at Time 2 (β = -0.09, <em>p</em> = 0.03). Post-hoc sensitivity analyses suggested unique effects when considering the number of types of CM experienced. Experiencing more types of CM was associated with greater Time 2 hs-CRP only when peer support was relatively lower (β = 0.07, <em>p</em> = 0.048). Additionally, youth who experienced more types of CM and who had higher levels of sibling support showed lower Time 2 hs-CRP (β = -0.15, <em>p</em> = 0.03). Overall, findings suggest that independent of CM history, greater sibling and peer support were associated with lower hs-CRP and BMI across a two-year period. Although there were no main effects of CM, greater peer support buffered the longitudinal effects of CM history on youth BMI. Additionally, in the context of experiencing multiple types of CM, greater levels of peer and sibling support functioned as protective factors.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106250"},"PeriodicalIF":7.6,"publicationDate":"2025-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissecting the genetic relationship between severe mental disorders and autoimmune diseases","authors":"Erik D. Wiström ,&nbsp;Julian Fuhrer ,&nbsp;Alexey Shadrin ,&nbsp;Vera Fominykh ,&nbsp;Kevin S. O’Connell ,&nbsp;Piotr Jaholkowski ,&nbsp;Nils Eiel Steen ,&nbsp;Sara E. Stinson ,&nbsp;Pravesh Parekh ,&nbsp;Oleksandr Frei ,&nbsp;Linn Rødevand ,&nbsp;Nadine Parker ,&nbsp;Jan Haavik ,&nbsp;Srdjan Djurovic ,&nbsp;Anders M. Dale ,&nbsp;Ole A. Andreassen ,&nbsp;Olav B. Smeland","doi":"10.1016/j.bbi.2025.106249","DOIUrl":"10.1016/j.bbi.2025.106249","url":null,"abstract":"<div><div>Severe mental disorders have been linked to immune system dysfunction. While a genetic association between mental disorders and autoimmune diseases has been suggested, their genetic relationship remains incompletely understood. Utilizing a complementary set of statistical analyses, we conducted a comprehensive investigation of the genetic architecture between severe mental disorders (major depression (MD), bipolar disorder (BD), and schizophrenia (SCZ)) and seven autoimmune diseases (autoimmune thyroiditis, celiac disease, inflammatory bowel disease (IBD), multiple sclerosis, psoriasis, rheumatoid arthritis, and type 1 diabetes), involving a total of 667,518 cases from 10 genome-wide association studies. While MD was positively genetically correlated with five autoimmune diseases, BD and SCZ were only positively correlated with IBD, suggesting differences in the genetic signal shared with autoimmunity across these mental disorders. A considerable fraction of genetic variants influencing autoimmune diseases (range 17.1–88.4 %) was estimated to overlap with mental disorders; however, this constitutes only a minor part of genetic variants influencing the more polygenic mental disorders. Finally, we identified 172 genetic loci jointly affecting mental disorders and autoimmune diseases, implicating both lipid metabolism and TNF signaling. In conclusion, MD, BD, and SCZ have a small but distinct genetic overlap with autoimmune diseases, which may inform new possible immune targets for treatment in mental illness.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106249"},"PeriodicalIF":7.6,"publicationDate":"2025-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deletion of the microglial phagocytic receptor MerTK mimics early-life adversity-induced changes in synapses and behavior in male mice","authors":"Madison M. Garvin ,&nbsp;Urjoshi Kar ,&nbsp;Cassandra L. Kooiker ,&nbsp;Jessica L. Bolton","doi":"10.1016/j.bbi.2025.106246","DOIUrl":"10.1016/j.bbi.2025.106246","url":null,"abstract":"&lt;div&gt;&lt;div&gt;Early-life adversity (ELA) is a significant risk factor for emotional disorders like depression, likely due to changes in stress-related circuit development. We have previously shown that ELA increases the number of excitatory synapses onto corticotropin-releasing hormone (CRH)-expressing neurons in the paraventricular nucleus (PVN) by decreasing microglial synapse engulfment. Here, we hypothesize that ELA induces microglial dysfunction via inhibition of the microglial phagocytic receptor, MerTK, thus resulting in the observed changes in synapses and stress-related behavior. To determine whether deleting MerTK in microglia phenocopies the effects of ELA, microglia-specific conditional knockout (m)MerTK-KO (CX3CR1-Cre&lt;sup&gt;+&lt;/sup&gt;::MerTK&lt;sup&gt;fl/fl&lt;/sup&gt;) mice were crossed with ‘wild-type’ (CX3CR1-Cre&lt;sup&gt;-&lt;/sup&gt;::MerTK&lt;sup&gt;fl/fl&lt;/sup&gt;) mice, and their litters were reared in either a control or ELA (induced by limited bedding and nesting) environment, from postnatal days (P)2–10. Excitatory synapses in the PVN were assessed at P10, microglial engulfment was assessed at P8, and adult offspring were tested in a behavioral battery to measure threat-response (known to be dependent on PVN-CRH+ neurons) and anxiety-like behavior, followed by acute restraint stress to measure the neuroendocrine stress response. Following ELA at P10, we find that excitatory, but not inhibitory, synapses in the PVN are increased in males, which is mimicked by mMerTK-KO in control males, but causes no further increase in ELA males. Correspondingly, ELA and mMerTK-KO decrease microglial engulfment of excitatory presynaptic terminals at P8 in males. In contrast, females already have higher numbers of excitatory synapses at baseline, and exhibit no further increase with ELA or mMerTK-KO. Remarkably, the pattern of threat-response behavior in males closely matches the excitatory synapses, with mMerTK-KO control males escaping more from the simulated predator threat in the looming-shadow threat task, similar to ELA males. Again, females do not show any significant changes due to ELA or mMerTK-KO in the threat-response, although they do exhibit ELA-induced changes in anxiety-like behavior. ELA provokes a greater corticosterone response to acute stress in males, but not females, although females were again already higher at baseline. In sum, our results demonstrate that ELA provokes decreased microglial engulfment during development, leading to increased excitatory synapses in the PVN and an increased active response to threat in the looming-shadow test in males only. Deleting MerTK specifically from microglia recapitulates both the synaptic and behavioral effects in control males, but does not have an effect in ELA males or control females, suggesting that the MerTK pathway is already inhibited by ELA in males and less active in females at baseline. Our work is the first to elucidate the mechanisms underlying the male-biased microglial dysfunction caused by ELA, with prom","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106246"},"PeriodicalIF":7.6,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural oscillations serving abstract reasoning are differentially associated with inflammatory markers in people with HIV","authors":"Tony W. Wilson ,&nbsp;Mikki Schantell ,&nbsp;Sarah M. Dietz ,&nbsp;Samantha H. Penhale ,&nbsp;Kellen M. McDonald ,&nbsp;Kyla R. De Luca ,&nbsp;Molly E. Voller ,&nbsp;Lan D. Volberding ,&nbsp;Olivia R. Carusi ,&nbsp;Lucy K. Horne ,&nbsp;Yasra Arif ,&nbsp;Ryan Glesinger ,&nbsp;Jason A. John ,&nbsp;Hannah J. Okelberry ,&nbsp;Pamela E. May-Weeks ,&nbsp;Adam J. Case ,&nbsp;Matthew C. Zimmerman ,&nbsp;Rachel K. Spooner","doi":"10.1016/j.bbi.2025.106236","DOIUrl":"10.1016/j.bbi.2025.106236","url":null,"abstract":"<div><h3>Introduction</h3><div>Despite living a normal lifespan, people with HIV (PWH) are at a much greater risk of developing cognitive impairment. While the precise mechanisms are not fully understood, persistently high inflammation levels are thought to be a key contributor, as multiple studies have linked cognitive impairment and elevated inflammation. In contrast, evidence of a relationship between neural function and inflammatory activity is extremely limited in PWH and/or controls. Thus, in the current study, we integrate state-of-the-art dynamic functional brain mapping with measures of three inflammatory markers that have been widely reported as elevated in PWH.</div></div><div><h3>Methods</h3><div>A total of 142 participants (range: 20–66 years old; 64 PWH and 78 controls) completed a validated abstract reasoning task during magnetoencephalographic (MEG) imaging, underwent comprehensive neuropsychological testing, and provided a blood sample for plasma-based inflammatory marker analysis of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interferon γ-induced protein 10 (IP-10). The two groups were matched on age, sex, race/ethnicity, body-mass index (BMI), handedness, anxiety, substance use, and common medical conditions such as diabetes. Oscillatory neural responses supporting abstract reasoning were imaged by applying a beamformer to the processed MEG data, and whole-brain, voxel-wise analyses were conducted using each individual’s CRP, TNF-α and IP-10 concentrations, controlling for age and BMI, to identify the differential impact of inflammation on oscillatory neural dynamics in PWH.</div></div><div><h3>Results</h3><div>PWH exhibited significantly higher levels on each of the three inflammatory markers and performed more poorly on the abstract reasoning task than matched controls, with CRP levels being significantly related to performance across all participants. Critically, TNF-α levels were significantly related to the strength of theta oscillations during abstract reasoning in the left inferior frontal gyrus, with higher TNF-α scaling with weaker theta and the strength of this relationship differing by group. A similar relationship among increasing CRP levels and decreasing gamma oscillations was found in the left inferior parietal cortices, while increasing CRP was also associated with decreasing gamma in the right dorsolateral prefrontal cortex across both groups, with the latter being coupled to behavioral performance in controls.</div></div><div><h3>Discussion</h3><div>These findings provide the first evidence linking elevated inflammatory levels to altered brain dynamics and performance in PWH. Such data provides crucial empirical evidence supporting the long-held view that elevated inflammation may be central to the higher rates of cognitive decline in PWH. Future work should examine whether decreasing these inflammatory levels leads to improvements in cognitive function in PWH.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106236"},"PeriodicalIF":7.6,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute ischaemic stroke alters the composition and function of circulating B cells","authors":"Mehwish Younas ,&nbsp;Harry R. Deijnen ,&nbsp;Ruth Stephens ,&nbsp;Alison Harris ,&nbsp;Thomas O. Williams ,&nbsp;Sabrina Tamburrano ,&nbsp;Ian E. Prise ,&nbsp;Craig J. Smith ,&nbsp;Stuart M. Allan ,&nbsp;Laura McCulloch ,&nbsp;John R. Grainger ,&nbsp;Barry W. McColl","doi":"10.1016/j.bbi.2025.106244","DOIUrl":"10.1016/j.bbi.2025.106244","url":null,"abstract":"<div><div>Distinct B cell populations are found in circulation, including those with innate-like properties, that have varied functions in pathogen protection, vaccination and immunoregulation. The effects of tissue injury on circulating B cell populations are poorly explored. Here we show that, following acute ischaemic stroke (AIS), a common cause of neurological disability associated with systemic immune dysfunction, the circulating B cell compartment has altered functionality, alongside marked reductions in marginal zone (MZ)-like B cells, an innate-like B cell subset. Of note, release of Immunoglobulin (Ig) M, a key innate-like B cell-derived factor important in anti-bacterial responses, and regulatory cytokines including IL-6 and IL-10, was impaired upon stimulation of sorted B cells from AIS patients. B cells express adrenergic receptors (ARs), in both control and AIS patients, and release of the β2-AR agonist noradrenaline (NA) is elevated acutely following stroke. <em>In vitro</em> exposure of B cells from healthy individuals to NA recapitulated some of the functional modulation observed in AIS patients. Moreover, increased cell death of MZ-like B cells was observed in response to NA. Secondary infection is a common post-stroke complication that could be responsible for altered B cell characteristics. However, in line with the impact of NA on B cell populations, alterations were largely driven by stroke rather than secondary infection. Taken together, these findings demonstrate that neuroimmune factors are an important signal that could rapidly modify defined B cell populations early after tissue injury and highlight altered innate-like B cell function as a previously unappreciated characteristic of the systemic immunological response to acute stroke.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106244"},"PeriodicalIF":7.6,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Social factors as buffers for the adverse impact of adverse childhood experiences on biological age acceleration among adults in Hispanic Community Health Study / Study of Latinos","authors":"Yinxian Chen ,&nbsp;Sarina Abrishamcar ,&nbsp;Jasmine K. Aqua ,&nbsp;Christian Dye ,&nbsp;Linda C. Gallo ,&nbsp;Maria M. Llabre ,&nbsp;Frank J. Penedo ,&nbsp;Carmen R. Isasi ,&nbsp;Krista M. Perreira ,&nbsp;Bharat Thyagarajan ,&nbsp;Martha Daviglus ,&nbsp;Amber Pirzada ,&nbsp;Andrea Baccarelli ,&nbsp;Karen N. Conneely ,&nbsp;Rebecca Jones-Antwi ,&nbsp;Shakira F. Suglia","doi":"10.1016/j.bbi.2025.106241","DOIUrl":"10.1016/j.bbi.2025.106241","url":null,"abstract":"<div><h3>Background</h3><div>This study examined whether social factors, including social support, social networks, and familism, modify the longitudinal association between ACEs and epigenetic age acceleration (EAA).</div></div><div><h3>Methods</h3><div>We analyzed DNA methylation (DNAm) profile data from two visits (approximately six years apart) among 960 Hispanic/Latino adults in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). GrimAge epigenetic age and DunedinPACE pace of aging were used. Linear mixed models examined effect modification of social support, social networks (network diversity and the number of embedded networks), and familism (family obligation, support, and as referents) on the association between high vs. low-to-moderate ACEs (i.e., ≥ 4 vs. &lt; 4 ACEs) and repeatedly measured EAA. Models adjusted for age, sex, parental education, childhood economic hardship, nativity, and cell-type proportions. We also dichotomized the levels of social support and both subscales of social networks to low (≤ 75th percentile) and high (&gt; 75th percentile), and assessed joint effect modification by social support and networks.</div></div><div><h3>Results</h3><div>The mean difference in GrimAge acceleration (AgeAccelGrim) between high and low-to-moderate ACEs was statistically significantly attenuated when social support levels were higher (β for interaction = -0.73 years; 95 % CI: −1.23, −0.24; p = 0.003). No evidence of effect modification was found for social networks or familism. Having only high social support (β for interaction = -1.40 years; 95 % CI: −2.79, −0.01; p = 0.049) or both high social support and network diversity (β for interaction = -1.57 years; 95 % CI: −2.72, −0.42; p = 0.008) significantly decreased the mean difference in AgeAccelGrim between high and low-to-moderate ACEs.</div></div><div><h3>Conclusion</h3><div>Social support may independently buffer the adverse impact of ACEs on biological age acceleration among Hispanic/Latino adults, and the buffering effect may be stronger when accompanied by diverse social networks.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"132 ","pages":"Article 106241"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation, metabolic dysregulation, and depression profiles related to anhedonia and atypical, energy-related symptoms","authors":"J.C. Zwiep ,&nbsp;F. Lamers ,&nbsp;C.H. Vinkers ,&nbsp;N.J.A. van der Wee ,&nbsp;B.W.J.H. Penninx ,&nbsp;L. Nawijn ,&nbsp;Y. Milaneschi","doi":"10.1016/j.bbi.2025.106240","DOIUrl":"10.1016/j.bbi.2025.106240","url":null,"abstract":"<div><h3>Introduction</h3><div>Depression manifests heterogenous bio-clinical profiles. Anhedonia has been previously linked to inflammation. Other research has associated inflammation and metabolic dysregulations with atypical, energy-related depressive symptoms (AES). In the present study, we examined the associations of inflammation and metabolic dysregulations with anhedonia and compared these associations with those of inflammation and metabolic dysregulations with AES, and with a negative control symptom profile, previously shown unrelated to inflammation and metabolic dysregulation.</div></div><div><h3>Methods</h3><div>Data was from 2,981 persons of the Netherlands Study of Depression and Anxiety (NESDA). Inflammatory markers included C-reactive protein (CRP), Interleukin-6 (IL-6), Tumor Necrosis Factor alpha (TNF-α), and glycoprotein acetyls. Metabolic markers were body mass index (BMI), waist circumference, triglycerides, high-density-lipoprotein cholesterol (HDL cholesterol), glucose and leptin. Anhedonia, AES and negative control symptom profiles were based on sum scores from different items from the Inventory of Depressive Symptomatology Self-Report (IDS-SR). The results were internally replicated in NESDA’s 6-year follow-up (N = 2,256).</div></div><div><h3>Results</h3><div>Anhedonia was positively associated with IL-6, glycoprotein acetyls, BMI, waist circumference, triglycerides, glucose, and leptin (β ranging from 0.063 to 0.122) and negatively associated with HDL cholesterol (β = -0.063). Associations were only partially explained by major lifestyle and health-related factors and confirmed at 6-year follow-up (<em>r</em> = 0.939 correlation between estimates at baseline and follow-up). AES showed highly consistent associations with the markers, with relatively larger effects as compared to anhedonia, while the negative control symptoms were linked only to higher glycoprotein acetyls.</div></div><div><h3>Conclusion</h3><div>Our results indicate consistent associations between several markers of inflammation and metabolic dysregulation with anhedonia and AES. Full characterization of depression profiles and their complex interrelations should be leveraged in future clinical research to select specific subgroup of depressed patients and develop more targeted treatment approaches.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"132 ","pages":"Article 106240"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural control of Immunotherapy: how Tumor-innervation shapes Anti-Tumor immune responses","authors":"Hatice Satilmis ,&nbsp;Adrien Denis ,&nbsp;Karin Vanderkerken ,&nbsp;Elke De Bruyne ,&nbsp;Eline Menu ,&nbsp;Erica K Sloan ,&nbsp;Kim De Veirman","doi":"10.1016/j.bbi.2025.106239","DOIUrl":"10.1016/j.bbi.2025.106239","url":null,"abstract":"<div><div>The role of the sympathetic nervous system (SNS) in cancer biology has gained increasing attention, and its ability to affect immunotherapy is starting to become clearer. Extensive evidence shows that neuro-onco-immune interactions significantly influence tumor progression and the effectiveness of cancer treatments. Blocking SNS signaling, primarily through β-adrenergic receptors, enhances immune cell functions, by increasing CD8⁺ T-cell activation and cytokine production, while reducing immunosuppressive cell populations.</div><div>This review explores the relationship between SNS signaling and cancer immunotherapy, emphasizing how SNS activation affects the efficacy of various immunotherapies, including immune modulators, immune checkpoint inhibitors, oncolytic virus therapy, therapeutic vaccines, and CAR-T cell therapies. We summarize retrospective studies investigating the use of β-blockers during immunotherapy, suggesting potential benefits for treatment outcomes of blocking SNS signaling in the tumor microenvironment. We examine ongoing clinical trials that evaluate the use of beta-blockers with immune checkpoint inhibitors, which aim to improve patient outcomes. While translational and preclinical studies provide ample evidence for targeting SNS signaling in cancer immunotherapy, clinical studies are only beginning to emerge. Ultimately, this review underscores the need for further research to better understand how SNS signaling can be targeted to optimize immunotherapy, paving the way for more effective treatment strategies.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"132 ","pages":"Article 106239"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increases in inflammation are associated with decreased trust of racial out-group members","authors":"Natalie M. Antenucci ,&nbsp;Mallory J. Feldman ,&nbsp;Tatum A. Jolink ,&nbsp;Taylor N. West ,&nbsp;Megan N. Cardenas ,&nbsp;Gabriella M. Alvarez ,&nbsp;Keely A. Muscatell","doi":"10.1016/j.bbi.2025.106242","DOIUrl":"10.1016/j.bbi.2025.106242","url":null,"abstract":"<div><div>While social group divisions occur naturally, inauspicious contexts like pathogen threat may exacerbate divides, driving in-group favoritism and out-group derogation. Minimal work has examined biological underpinnings of intergroup dynamics, particularly immune changes likely to accompany pathogen threat. To address this, we administered the influenza vaccine to 44 young adult participants. Before and after receiving the vaccine, participants completed a modified affect misattribution procedure, wherein they rated the trustworthiness of racial in-group and out-group faces. Participants also provided pre- and post-vaccine blood samples which were assayed for the inflammatory cytokine interleukin-6 (IL-6). Results showed a negative association between inflammatory reactivity and ratings of out-group faces: those who experienced greater increases in IL-6 rated racial out-group faces as less trustworthy than those with less IL-6 reactivity. This work begins exploring the role of inflammation in intergroup processes and findings, while preliminary, suggest a novel biological process that is associated with intergroup perception.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106242"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Using social risk factors to predict allostatic biotypes of depression: A latent profile and multinomial regression analysis","authors":"Jay O’Shields ,&nbsp;Helisha Soni ,&nbsp;Orion Mowbray","doi":"10.1016/j.bbi.2025.106243","DOIUrl":"10.1016/j.bbi.2025.106243","url":null,"abstract":"<div><h3>Objective</h3><div>Major depression is often difficult to treat, particularly among individuals exposed to psychosocial risks like childhood maltreatment, loneliness, and recent stress. These experiences may lead to biological dysregulation consistent with allostatic load theory. This study explored whether distinct biological profiles among adults with depression are associated with specific psychosocial and health-related factors.</div></div><div><h3>Method</h3><div>Data were drawn from the Midlife in the United States study (MIDUS), including 367 participants with clinically significant depressive symptoms (CES-D ≥ 16). Latent profile analysis identified biological profiles based on 23 biomarkers across seven systems: inflammation, glucose, sympathetic and parasympathetic nervous systems, HPA-axis, cardiovascular, and lipids. Multinomial regression models examined associations between profile membership and psychosocial (childhood maltreatment, loneliness, recent stress), health (alcohol use, smoking, exercise), and demographic variables (sex, race/ethnicity, age, education).</div></div><div><h3>Results</h3><div>A five-profile solution best fit the data: High Inflammation &amp; Glucose (<em>n</em> = 74), Low PNS (<em>n</em> = 83), High PNS (<em>n</em> = 73), Healthy Depression (<em>n</em> = 67), and High HPA-Axis (<em>n</em> = 70). Childhood maltreatment significantly predicted membership in the High Inflammation &amp; Glucose and Low PNS profiles compared to the Healthy Depression group, even after controlling for health behaviors and demographics. Loneliness and recent stress were not significant predictors.</div></div><div><h3>Conclusion</h3><div>Childhood maltreatment is a predictor of biological dysregulation in depression, differentially predicting profiles characterized by inflammatory and metabolic vs parasympathetic functioning. These may represent different vulnerability pathways from social experiences to depressive illness. Incorporating measurement strategies specific to these pathways may aide in selecting treatment options for people who have depression and a history of childhood maltreatment.</div></div>","PeriodicalId":9199,"journal":{"name":"Brain, Behavior, and Immunity","volume":"133 ","pages":"Article 106243"},"PeriodicalIF":7.6,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145826944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}