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• High expression of IL-17A promotes the growth and metastasis of many tumors, leading to a poor prognosis for cancer patients. • IL-17A promotes resistance to anti-PD-1 therapy by increasing PD-L1 expression in patients with various cancers, and combined anti-IL-17A and anti-PD-1 therapy can significantly improve efficacy. • IL-17A levels in cancer patients may be a predictor of the efficacy of combination therapy. Interleukin 17A (IL-17A) is a major member of the IL-17 cytokine family and is produced mainly by T helper 17 (Th17) cells. Other cells such as CD8+ T cells, γδ T cells, natural killer T cells and innate lymphoid-like cells can also produce IL-17A. In healthy individuals, IL-17A has a host-protective capacity, but excessive elevation of IL-17A is associated with the development of autoimmune diseases and cancer. Monoclonal antibodies (mAbs) targeting IL-17A (e.g., ixekizumab and secukinumab) or IL-17A receptor (IL-17RA) (e.g., brodalumab) would be investigated as potential treatments for these diseases. Currently, the application of IL-17A-targeted drugs in autoimmune diseases will provide new ideas for the treatment of tumors, and its combined application with immune checkpoint inhibitors has become a research hotspot. This article reviews the mechanism of action of IL-17A and the application of anti-IL-17A antibodies, focusing on the research progress on the mechanism of action and therapeutic blockade of IL-17A in various tumors such as colorectal cancer (CRC), lung cancer, gastric cancer and breast cancer. Moreover, we also include the results of therapeutic blockade in the field of cancer as well as recent advances in the regulation of IL-17A signaling. [ABSTRACT FROM AUTHOR]

• CD226 expression was up-regulated on NK cells and T cell subsets in tuberculosis patients. • CD226+-CD3+CD8+ T cells might be a potential predictor of tuberculosis occurrence. • CD226+-CD3+CD4+ T cells and -CD56dimCD16+ NK cells displayed a higher level of IFN-γ, and CD226+-CD3+CD4+, -CD3+CD8+T cells and -CD56dimCD16+ NK cells displayed a higher level of CD107a production from tuberculosis patients. • CD226+-CD3+CD4+ T cells and CD56dimCD16+ NK cells tended to mediate cytotoxicity for disease progression. Human T cells and natural killer (NK) cells are major effector cells of innate immunity exerting potential immune surveillance against tuberculosis infection. CD226 is an activating receptor playing vital roles in the functions of T cells and NK cells during HIV infection and tumorigenesis. However, CD226 is a less-studied activating receptor during Mycobacterium tuberculosis (Mtb) infection. In this study, we used peripheral blood from tuberculosis patients and healthy donors to evaluate CD226 immunoregulation functions from two independent cohorts using Flow cytometry. Here, we found that a subset of T cells and NK cells that constitutively express CD226 exhibit a distinct phenotype in TB patients. In fact, the proportions of CD226+ and CD226- cell subsets differ between healthy people and tuberculosis patients, and the expression of immune checkpoint molecules (TIGIT, NKG2A) and adhesion molecules (CD2, CD11a) in CD226+ and CD226- subsets of T cells and NK cells exhibits special regulatory roles. Furthermore, CD226+ subsets produced more IFN-γ and CD107a than CD226- subsets in tuberculosis patients. Our results imply that CD226 may be a potential predictor of disease progression and clinical efficacy in tuberculosis by mediating the cytotoxic capacity of T cells and NK cells. [ABSTRACT FROM AUTHOR]

• The immune microenvironment is emerging as a determinant of cervical cancer treatment. • The expression of B cells and PD-L1 increased after treatment with PD-1 inhibitors. • B cells may play a role in cervical cancer immunotherapy. This study evaluated the basic immune status of cervical cancer and the influences of immunotherapy on the immune microenvironment, and analyzed the correlation between changes in the immune microenvironment and prognosis. We retrospectively analyzed the treatment status of 8 patients with advanced recurrent cervical cancer treated with PD-1 inhibitors and detected the tumor-infiltrating immune markers (CD3, CD4, CD8, CD20, CD56, CD68, PD-1, and PD-L1) by immunohistochemistry. All patients showed good tolerance during the treatment. Complete response (CR), partial response (PR) and stable disease (SD) was observed in 3, 2, and 3 patients, respectively. Immunohistochemical analysis showed immunotherapy resulted in increased infiltration of T lymphocytes, natural killer cells, and B cells, especially among those who responded well. The expression of B cells in 4 of the 5 patients with clinical benefit was relatively high, and the expression of PD-L1 in these 5 patients showed a combined positive score > 3. PD-L1 expression increased significantly after treatment with PD-1 inhibitors. Second-generation sequencing showed that the tumor mutation burden of two patients with adenocarcinoma was high, and after immunotherapy, one case recurred after cure and the other remained stable. PR was also observed in squamous cell carcinoma patients with dMMR (p.R2165H/c.6494G > A) and PIK3CA (p.E545K(E9)) mutations. The expression of B cells and PD-L1 has certain predictive effect for the efficacy of immunotherapy in cervical cancer under the condition of high or low T cell infiltration, and can inform treatment decision-making for patients with advanced cervical cancer. [ABSTRACT FROM AUTHOR]