Immunology最新文献

Psychological stress has been linked to increased incidence and mortality of cancer. During stress, cortisol is released into circulation and regulates cellular processes including immune activity by acting on glucocorticoid receptors (GCRs) expressed by target cells. Chronic stress-induced cortisol has been suggested to promote tumour progression and compromise the efficacy of cancer treatments. Conversely, cortisol is also transiently secreted during exercise. Although exercise has been suggested to have beneficial effects against cancer, the impact of exercise-elevated cortisol on immune cell functions remains poorly understood. Here we studied the dynamics of cortisol secretion following exercise and how cortisol affects effector functions of T cells in the context of acute versus chronic stress. We show that 40 min of acute, high-intensity exercise in healthy adults significantly increased stable circulating cortisol levels whereas a 5-min sprint failed to. Acute exposure to cortisol for 4 h showed no negative effects on the proliferation, cytokine release, or killing activity of human CD3⁺ T cells. In contrast, chronic cortisol dampened these T cell effector functions. Furthermore, chronic cortisol exposure induced the proliferation of several cancer cell lines. Our findings highlight the opposing effects of cortisol during acute stress, such as exercise, compared to chronic stress, on cancer cells and T cells. This suggests an important potential in targeting cortisol signalling to enhance cancer immunotherapy.

A paper of Matsumoto and colleagues [1] is highly relevant for mucosal immunology as it presents new data of bronchus-associated lymphoid tissue (BALT) in humans. In 1972, John Bienenstock and colleagues [2] described the aggregation of lymphoid tissue in the bronchial wall and introduced the term BALT. Those investigations were restricted to rabbits but soon this concept was included in many textbooks and BALT was described as a secondary lymphoid tissue comparable to Peyer's patches [3]. Nevertheless, in the lungs of normal human adults BALT was absent [4]. In contrast, BALT was detected in 8% of chronically inflamed human lungs [5]. In young children who died of SIDS or other reasons BALT was documented in about 40% [6]. In 2024, we documented that also in rabbits, BALT is dependent on environmental stimuli [7]. Later, inducible BALT (iBALT) was described by a couple of groups [8-10]. These structures seem to fulfil the criteria for a tertiary lymphoid tissue. However, not all of the reported follicular aggregations of lymphoid cells were located in the bronchial wall and then the term bronchus-associated was not applicable. The recent data of Matsumoto et al. [11] support old findings of arising and dissolving of BALT in humans and support our two-step concept: Stimulation by external stimuli to re-induce BALT and then inhalation of vaccines to produce protective antibodies.

The authors declare no conflicts of interest.

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

Tissue-resident memory T (T_RM) cells are a specialised subset of immune cells that remain within tissues, playing a vital role in localised immune defence and long-term immunity. Unlike circulating memory T cells, T_RM cells do not recirculate to provide rapid and effective responses against previously encountered pathogens at the tissue level. The formation of T_RM cells is driven by tissue-specific cues, guiding their differentiation and retention within organs such as the skin, lungs and gut. They are characterised by the expression of unique markers, including CD69 and CD103, which facilitate their retention and longevity in tissues. T_RM cells are essential for immune surveillance, effectively detecting and responding to different infections and contributing to tumour suppression. However, T_RM cells are also implicated in chronic inflammatory and autoimmune diseases, where persistent activation by resident and autoantigens can lead to tissue damage. This pathogenic role is evident in chronic inflammatory conditions such as psoriasis, vitiligo and inflammatory bowel disease (IBD), where T_RM cells may drive persistent localised inflammation and contribute to disease progression and severity. Emerging therapeutic strategies seek to modulate T_RM cells to balance their protective and pathogenic roles in these inflammatory diseases. Approaches such as checkpoint inhibitors, cytokine modulation and cell-depletion therapies aim to enhance T_RM cells' beneficial immune functions while minimising their role in autoimmunity. A deeper understanding of T_RM cell development, maintenance and functional diversity is critical for advancing treatments for infectious diseases, chronic inflammation, autoimmune conditions and cancer.

Cutaneous leishmaniasis (CL), a neglected tropical disease prevalent in Brazil, is caused by Leishmania braziliensis ( L. braziliensis ) and is marked by ulcerative skin lesions and an exacerbated Th1-driven inflammatory response. This study investigates the therapeutic potential of oral tolerance (OT) induced by a genetically modified strain of Lactococcus lactis ( L. lactis ) producing heat shock protein 65 (HSP65) from Mycobacterium leprae in a murine model of CL. BALB/c mice were infected with L. braziliensis and treated orally with HSP65-producing L. lactis or control L. lactis (empty vector) for four consecutive days, starting at 4 weeks post-infection. Mice receiving HSP65-producing L. lactis showed reduced lesion size and parasite burden. Cytokine analysis in draining lymph nodes revealed a shift from a pro-inflammatory IFN-γ response to an increased IL-10 production, correlating with milder inflammation and less tissue damage. Additionally, the treatment promoted an increase in regulatory T cells (Tregs), including CD4⁺CD25⁺FOXP3⁺ and CD4⁺LAP⁺ (membrane-associated TGF-β) cells in the draining lymph nodes. This therapeutic effect was not observed in a more severe model of CL using Leishmania major. This study underscores the potential of oral tolerance induction using HSP65-producing L. lactis as a promising immunoregulatory therapeutic approach for some chronic inflammatory infections, mainly those that display a primed balance in immune response.

J. A. Chaves de Souza, S. C. T. Frasnelli, F. d. A. Curylofo-Zotti, M. J. Ávila-Campos, L. C. Spolidório, D. S. Zamboni, D. T. Graves, and C. Rossa Jr, “NOD1 in the Modulation of Host–Microbe Interactions and Inflammatory Bone Resorption in the Periodontal Disease Model,” Immunology 149, no. 4 (2016): 374–385, https://doi.org/10.1111/imm.12654.

Concerns were raised by a third party regarding duplicated image panels between this article (Figure 1a, WT PBS and Aa panels; 1b WT Aa panel; and 2a WT PBS and Aa+Lf), and two other previously published articles by the same group of authors.

As stated by the authors, the subpanels in question either represent unintentional reuse of images to depict the same positive and negative control experimental conditions or may reflect image compilation errors in the subsequently published articles. However, appropriate citation to this original article was inadvertently omitted. The authors have acknowledged these issues and are taking steps to address them with the relevant journals.

In addition, the authors acknowledged that an incorrect image was used for Figure 1b bottom left image, Nod1 KO—Aa subpanel, which does not represent the intended experimental condition. They have provided the corresponding raw data to support their explanation and have prepared a corrected version of the figure.

The corrected Figure 1b bottom left image is provided below.

M. Koganesawa, D. F. Dwyer, K. Alhallak, J. Nagai, K. Zaleski, S. Samuchiwal, et al., “Pla2g5 Contributes to Viral-Like-Induced Lung Inflammation Through Macrophage Proliferation and LA/Ffar1 Lung Cell Recruitment,” Immunology 172, no. 1 (2024): 144–162, https://doi.org/10.1111/imm.13766.

In the article, there are labeling errors in Figures 1, 6 and 7.

We apologise for these errors.

Immunotherapy has demonstrated groundbreaking clinical efficacy across diverse cancer types. Nevertheless, its therapeutic potential remains constrained, with only a small subset of patients achieving durable clinical responses. Emerging evidence highlights tertiary lymphoid structures (TLSs), ectopic lymphoid aggregates induced by chronic inflammation or malignancy, play critical roles in mediating positive responses to cancer immunotherapy. Currently, there is a notable absence of comprehensive systematic evaluations that synthesise both clinical and preclinical experimental data regarding the role of TLSs in enhancing cancer immunotherapy. In this review, we examined the composition of TLSs and elucidated how their heterogeneity influences cancer treatment outcomes, with implications for both clinical practice and translational research. Furthermore, we emphasised the role of T follicular helper cells-mediated positive selection of germinal centre B cells in driving high-affinity antibody production. Additionally, we comprehensively analysed the effects of pharmacological agents, oncolytic viruses, adeno-associated viruses and biomaterials on TLSs formation and highlighted their capacity to potentiate immune checkpoint inhibitor responses. Consequently, targeting TLSs is a promising strategy for enhancing the positive response to cancer immunotherapy.