International Reviews of Immunology最新文献

Acute bronchiolitis caused by the respiratory syncytial virus triggers an inflammatory response with the production and release of several pro-inflammatory cytokines. Evidence suggests that their levels are associated with the severity of the infection. This systematic review and meta-analysis aim to assess whether the levels of TNF-α and IFN-γ are associated with the severity of acute viral bronchiolitis. We searched MEDLINE libraries (via PUBMED), EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), Scientific Electronic Library Online (SciELO), Latin American Caribbean Health Sciences Literature (LILACS), Cumulative Index to Nursing and Allied Health Literature (CINAHL), Web of Science, and the gray literature through April 2020. Random effect models were used for general and subgroup analysis. In total, six studies were included with a total of 744 participants. The mean TNF-α levels between the severe group did not differ from the control group 0.14 (95% CI: -0.53 to 0.82, I² = 91%, p < 0.01); the heterogeneity was high. The results remained insignificant when the analyses were performed including only studies with high quality 0.25 (95% CI: -0.46 to 0.96, I² = 92%, p < 0.01) I² = 95%, p = 0.815), when TNF-α was nasal 0.60 (95% CI: -0.49 to 1.69), I² = 94%, p < 0.01), or serum -0.08 (95% CI: -0.48 to 0.31), I² = 29%, p = 0.24). In the analysis of studies measuring IFN-γ, there was also no significance of -0.67 (95% CI: -1.56 to 0.22, I² = 76%, p = 0.04). In conclusion, this meta-analysis suggests that the most severe patients do not have different mean TNF-α and IFN-γ values ​than patients with mild disease, but the heterogeneity of the studies was high. Supplemental data for this article is available online at https://doi.org/10.1080/08830185.2021.1889534.

The pandemic causing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has globally infected more than 50 million people and ∼1.2 million have succumbed to this deadly pathogen. With the vaccine trials still in clinical phases, mitigation of Coronavirus Disease 2019 (COVID-19) relies primarily on robust virus detection methods and subsequent quarantine measures. Hence, the importance of rapid, affordable and reproducible virus testing will serve the need to identify and treat infected subjects in a timely manner. Based on the type of diagnostic assay, the primary targets are viral genome (RNA) and encoded proteins. Currently, COVID-19 detection is performed using various molecular platforms as well as serodiagnostics that exhibit approximately 71% sensitivity. These methods encounter several limitations including sensitivity, specificity, availability of skilled expertise and instrument access. Saliva-based COVID-19 diagnostics are emerging as a superior alternative to nasal swabs because of the ease of sample collection, no interaction during sampling, and high viral titers during early stages of infection. In addition, SARS-CoV-2 is detected in the environment as aerosols associated with suspended particulate matter. Designing virus detection strategies in diverse samples will allow timely monitoring of virus spread in humans and its persistence in the environment. With the passage of time, advanced technologies are overcoming limitations associated with detection. Enhanced sensitivity and specificity of next-generation diagnostics are key features enabling improved prognostic care. In this comprehensive review, we analyze currently adopted advanced technologies and their concurrent use in the development of diagnostics for SARS-CoV-2 detection.

Chronic inflammation has emerged as a key player at different stages of cancer development. A prominent signaling pathway for acute and chronic inflammation is the activation of the caspase-1 inflammasomes. These are complexes that assemble on activation of certain nucleotide-binding domain, leucine-rich repeat containing proteins (NLRs), AIM2-like receptors (ALRs), or pyrin due to activation via PAMPs or DAMPs. Of these, five complexes-NLRP1, NLRP3, NLRC4, Pyrin, and AIM2 are of importance in the context of cancer for their activities in modulating immune responses, cell proliferation, and apoptosis. Inflammasomes have emerged as clinically relevant in multiple forms of cancer making them highly promising targets for cancer therapy. As lungs are a tissue niche that is prone to inflammation owing to its exposure to external substances, inflammasomes play a vital role in the development and pathogenesis of lung cancer. Therefore, manipulation of inflammasome by various immunomodulatory means could prove a full-proof strategy for the treatment of lung cancer. Here, in this review, we tried to explore the various strategies to target the inflammasomes for the treatment of lung cancer.

Interleukin (IL)-27, a member of the IL-6/IL-12 family, has an important role in modulating inflammation in partnership with innate and adaptive immune cells. IL-27 binding to IL-27R starts downstream signaling based on the target cells. It can instigate inflammation by inducing CD4⁺ T cell proliferation, Th1 polarization, cytotoxic T cell activation, generation of the natural killer cell, and macrophage and dendritic cell activation. However, by inducing programmed cell death and suppression of effector cells, IL-27 can suppress inflammation and return the immune response to hemostasis. Altogether, IL-27 displays multifaceted dual functions, which may result in either pro- or anti-inflammatory effects. Recent investigations indicated the antitumor activity of IL-27 via inducing Th1, and CTL responses and generating NK cells. On the other hand, IL-27 also can promote tumor cells' proliferation, survival, and angiogenesis. In the present review, we'll discuss recent advances concerning the role of IL-27 in inflammatory diseases such as infections, autoimmune diseases with a focus on cancer.

Semaphorin 4D (Sema4D) is a classic member of the semaphorin family involved in axonal guidance processes. The key effects of Sema4D in neurons are mediated by high affinity plexin receptors and are associated with cytoskeleton rearrangement, leading to growth cone collapse or regulation of cell migration. Along with this, the semaphorin is widely represented in the immune system and has a pronounced immunoregulatory activity. The involvement of Sema4D in the control of immune cell migration was shown almost twenty years ago, in one of the first studies of semaphorin. The emergence of such work was quite predictable, since the most well-known effects of Sema4D outside the immune system were associated precisely with the control of cell motility. However, after identification of CD72 as a specific Sema4D receptor in the immune system, studies of the immunoregulatory activity of semaphorin focused on its CD72-dependent effects unrelated to cytoskeleton rearrangement, and this trend continues up to now. Nevertheless, a number of recent studies demonstrating the presence of plexin receptors for Sema4D in the immune system forces us to return to the question of whether this semaphorin can play its classic role of a guidance molecule in relation to immune cells too. The review discusses Sema4D involvement in the control of immune cell migration, as well as the mechanisms of these effects and their potential contribution to the development and function of immune system.

SARS-CoV-2 is the causative agent of the COVID-19 pandemic. This novel coronavirus emerged in China, quickly spreading to more than 200 countries worldwide. Although most patients are only mildly ill or even asymptomatic, some develop severe pneumonia and become critically ill. One of the biggest unanswered questions is why some develop severe disease, whilst others do not. Insight on the interaction between SARS-CoV-2 and the immune system and the contribution of dysfunctional immune responses to disease progression will be instrumental to the understanding of COVID-19 pathogenesis, risk factors for worst outcome, and rational design of effective therapies and vaccines. In this review we have gathered the knowledge available thus far on the epidemiology of SARS-COV-2 infection, focusing on the susceptibility of older individuals, SARS-CoV-2-host cell interaction during infection and the immune response directed at SARS-CoV-2. Dendritic cells act as crucial messengers linking innate and adaptative immunity against viral infections. Thus, this review also brings a focused discussion on the role of dendritic cells and their immune functions during SARS-CoV-2 infection and how immune evasion strategies of SARS-CoV-2 and advancing age mediate dendritic cell dysfunctions that contribute to COVID-19 pathogenesis and increased susceptibility to worst outcomes. This review brings to light the hypothesis that concomitant occurrence of dendritic cell dysfunction/cytopathic effects induced by SARS-CoV-2 and/or aging may influence disease outcome in the elderly. Lastly, a detailed discussion on the effects and mechanisms of action of drugs currently being tested for COVID-19 on the function of dendritic cells is also provided.

Bladder cancer (BCa) is one of the most frequent urogenital malignancies which is mainly observed among men. There are various genetic and environmental risk factors associated with BCa progression. Transurethral endoscopic resection and open ablative surgery are the main treatment options for muscle invasive BCa. BCG therapy is also employed following the endoscopic resection to prevent tumor relapse. The tumor microenvironment is the main interaction site of tumor cells and immune system in which the immune cells are recruited via chemokines and chemokine receptors. In present review we summarized the main chemokines and chemokine receptors which have been associated with histopathological features of BCa patients in the world. This review highlights the chemokines and chemokine receptors as critical markers in early detection and therapeutic purposes among BCa patients and clarifies their molecular functions during BCa progression and metastasis.

In addition to generating effective immunity against infectious agents, the immune system helps to fight against different noninfectious human diseases while maintaining the balance between self and non-self discrimination. The breakdown of tolerance in autoimmune diseases or sustainable tolerance in an abnormal microenvironment such as chronic inflammation may initiate the process of malignancy. Immune system regulation is controlled by a complex, dynamic network of cells and mediators. Understanding the cellular and molecular basis of immune regulation provides better insight into the mechanisms governing the immune pathology of diseases. Among several cellular subsets and mediators with regulatory roles, a subpopulation of CD4⁺ T cells was recently reported to be positive for FoxP3 and negative for CD25, with a suggested range of functional activities in both cancer and autoimmune diseases. This CD4 subset was first reported in 2006 and thought to have a role in the pathogenesis of cancer. However, the spectrum of roles played by this T cell subset is broad, and no consensus has been reached regarding its immunological functions. In this review, we focused on the possible origin of CD4⁺CD25^‒FoxP3⁺ T cells and their function in cancer and autoimmune diseases.