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We recently reported that blockade of IL-10 signalling at the time of a human papillomavirus (HPV) long E7 peptide/LPS immunization leads to the regression of established HPV-16 immortalized tumours in mice similar to that induced by long E7 peptide/incomplete Freund’s adjuvant (IFA)-based vaccination. In this paper, we demonstrated that blockade of IL-10 signalling at the time of long E7 peptide/LPS could elicit stronger T cells responses and render the tumour more accessible for immune cell infiltration than vaccination with long E7 peptide/IFA. Furthermore, priming with long E7 peptide/LPS and IL10 signalling blockade then boosting with long E7 peptide/IFA elicits stronger CD8+ T cell responses than long E7 peptide/IFA immunization. The results suggest that priming with long E7 peptide/LPS and IL10 signalling inhibitor, then boosting with long E7 peptide/IFA elicits may lead to better HPV infection related tumour regression in clinic. [ABSTRACT FROM AUTHOR]

• In this paper, by reviewing MC phagocytic function, activated MC expression of APC surface markers, and MC participation in the inflammatory response and local renal immune response, we confirm that activated MCs can act as APCs in renal disease. • This review introduces MC function through a developmental perspective and summarizes the important role of MC as antigen-presenting cells in renal local immune response. • This review mentions the uniqueness of MC and also points out the limitations of MC research at this stage. Mesangial cells (MCs), as resident cells of the kidneys, play an important role in maintaining glomerular function. MCs are located between the capillary loops of the glomeruli and mainly support the capillary plexus, constrict blood vessels, extracellular matrix components, produce cytokines, and perform phagocytosis and clearance of macromolecular substances. When the glomerular environment changes, MCs are often affected, which can lead to functional transformation. The immune response is involved in the occurrence and development of various kidney diseases, in these diseases, antigen-presenting cells (APCs) play an important role. APCs can present antigens to T lymphocytes, causing them to become activated and proliferate. Studies have shown that MCs have phagocytic function and express APC markers on the cell surface. Additionally, MCs are stimulated by or produce various inflammatory factors to participate in the renal inflammatory response. Therefore, MCs have potential antigen presentation function and participate in the pathological changes of various kidney diseases as APCs upon activation. In this paper, by reviewing MC phagocytic function, activated MC expression of APC surface markers, and MC participation in the inflammatory response and local renal immune response, we confirm that activated MCs can act as APCs in renal disease. [ABSTRACT FROM AUTHOR]

• Platelet specific CD4+ T cells are required for anti-platelet antibody production. • Th1/Th2 immune deviation is directly implicated in ITP development and progression. • Th17 cells and platelets have multifaceted and pro-active mutual relationship. • Both numerical and functional abnormalities of Tregs were observed in ITP patients. • Th22, Th9 and Tfh cells could be also associated with ITP pathophysiology. Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet counts due to enhanced platelet clearance and compromised production. Traditionally, ITP was regarded a B cell mediated disorder as anti-platelet antibodies are detected in most patients. The very nature of self-antigens, evident processes of isotype switching and the affinity maturation of anti-platelet antibodies indicate that B cells in order to mount anti-platelet immune response require assistance of auto-reactive CD4+ T cells. For a long time, ITP pathogenesis has been exclusively reviewed through the prism of the disturbed balance between Th1 and Th2 subsets of CD4+ T cells, however, more recently new subsets of these cells have been described including Th17, Th9, Th22, T follicular helper and regulatory T cells. In this paper, we review the current understanding of the role and immunological mechanisms by which CD4+ T cells contribute to the pathogenesis of ITP. [ABSTRACT FROM AUTHOR]