2014年6月30日訊 /生物谷BIOON/--康奈爾大學的研究人員已經發現了一種免疫系統細胞可以在骨髓移植後，防止受體患者身體進攻供體細胞，受體患者身體進攻供體細胞的情況稱為移植物抗宿主反應（GVHD）。
這些免疫細胞稱為固有記憶型CD4 + T-細胞，能生成一種蛋白質抑制免疫系統，使其免於攻擊新引入的組織。在骨髓移植情況下，醫生嘗試匹配捐贈者和患者的組織類型，但它可能很難找到一個精確匹配。因此，患者通常需要免疫抑制藥物，其具有這樣的副作用如肝、腎損害和整體免疫系統缺陷。
發布在Journal of Immunology雜誌上的新研究確定了調控移植物抗宿主反應的特殊免疫細胞。研究人員希望研究結果會導致識別、並可能促進這些細胞存在的新方法。這項研究指出了一個「路線圖」，為臨床醫生試圖避免移植物抗宿主反應指明了方向。研究人員支出：如果這些細胞確實存在，這些患者將受到保護，免於發生移植物抗宿主反應；如果可以提高這類細胞的存在，就可以抑制移植物抗宿主反應。（生物谷Bioon.com）
Dendritic Cell–MHC Class II and Itk Regulate Functional Development of Regulatory Innate Memory CD4+ T Cells in Bone Marrow Transplantation
Weishan Huang，et al.
MHC class II (MHCII)-influenced CD4+ T cell differentiation and function play critical roles in regulating the development of autoimmunity. The lack of hematopoietic MHCII causes autoimmune disease that leads to severe wasting in syngeneic recipients. Using murine models of bone marrow transplantation (BMT), we find that MHCII?/?→wild-type BMT developed disease, with defective development of innate memory phenotype (IMP, CD44hi/CD62Llo) CD4+ T cells. Whereas conventional regulatory T cells are unable to suppress pathogenesis, IMP CD4+ T cells, which include conventional regulatory T cells, can suppress pathogenesis in MHCII-/-→wild-type chimeras. The functional development of IMP CD4+ T cells requires hematopoietic but not thymic MHCII. B cells and hematopoietic CD80/86 regulate the population size, whereas MHCII expression by dendritic cells is sufficient for IMP CD4+ T cell functional development and prevention of pathogenesis. Furthermore, the absence of Tec kinase IL-2-inducible T cell kinase in MHCII-/- donors leads to preferential development of IMP CD4+ T cells and partially prevents pathogenesis. We conclude that dendritic cells-MHCII and IL-2-inducible T cell kinase regulate the functional development of IMP CD4+ T cells, which suppresses the development of autoimmune disorder in syngeneic BMTs.