Rheumatoid arthritis is an autoimmune disease that primarily affects the limbs, but the pathogenic mechanism remains unclear. cd T cells, a T-cell subpopulation, are characterized by multiple biological functions and associated with a variety of diseases. This study investigated the antigen-presenting effects of cd T cells and their relationship with rheumatoid arthritis development. We found that Vc9Vd2 T cells (the predominant subtype of cd T cells in peripheral blood) were activated by isopentenyl pyrophosphate to continuously proliferate and differentiate into effector memory cells. The effector memory Vc9Vd2 T cells exhibited phenotypic characteristics of specific antigen-presenting cells, including high HLA-DR and CD80/86 expression. These Vc9Vd2 T cells could present soluble antigens and synthetic peptides to CD41 T cells. Vc9Vd2 T cells with different phenotypes showed different cytokine secretion patterns. Effector memory Vc9Vd2 T cells simultaneously secreted not only interferon (IFN)-c but also IL-17. The peripheral blood and joint synovial fluid from RA patients contained numerous heterogeneous cd T cells that were predominantly effector memory Vc9Vd2 T cells with the ability to secrete inflammatory factors. We also found that cd T cells had a similar antigen-presenting capability to B cells. These results suggest that during the development of rheumatoid arthritis, cd T cells can aggravate immune dysfunction and produce abnormal immune damage by secreting cytokines and inducing inflammatory cells to participate in synergistic inflammatory responses. Furthermore, cd T cells can behave similarly to B cells to present viral peptides and autoantigen peptides to CD4 1 T cells, thus sustaining CD4 1 T-cell activation.

Our results demonstrate that ACML-55 therapy can enhance function in immune surveillance in colon cancer-bearing mice through regulating both innate and adaptive immune responses.

Multiple myeloma (MM) is a plasma cell dyscrasia characterized by bone lesions and production of a paraprotein. B-lymphocyte stimulator (BLyS) and its receptor (BAFFR) were highly expressed on peripheral blood and bone marrow B cells in MM patients as compared to those with monoclonal gammopathy of unknown significance (MGUS) and healthy donors. Serum BLyS levels in MM patients were significantly higher than those in MGUS patients and healthy controls. BLyS expression was increased in bone marrow specimens from MM patients as ascertained by immunofluorescence. Furthermore, BLyS, together with IL-2 and IL-6, significantly promoted MM cell proliferation and BLyS receptor expression compared with that in the control group. Treatment with bortezomib, a therapeutic proteasome inhibitor induced apoptosis and repressed the proliferation of RPMI8226 and U266 cells through inhibition of NF-κB p65 and IκBα. These findings suggest that BLyS is involved in the immunopathogenesis of MM and may prove to be a hallmark of MM.