(一)B细胞在自身免疫性疾病。B细胞已经锁定,antibody-independent致病功能。自身抗体分泌特定受体或受体配体可以激活或抑制受体的功能。免疫复合物沉积可以激活补体和效应细胞。自身抗体可以绑定到基本结构分子和干扰结构元素的合成,促进抗原的吸收。独立于抗体分泌的B细胞分泌促炎细胞因子,支持异位gc的形成,作为抗原呈递细胞。自身抗体分泌和BCR B细胞可以调节抗原的处理和显示,从而影响了t细胞的本质因素。(b)致病性免疫复合物沉积的影响。Fc的部分抗体免疫复合物可以绑定的C1q补体经典,最终导致C5a和C3a的释放。这些过敏毒素促进释放促炎细胞因子,作为化学引诱物的效应细胞。 Moreover they induce the upregulation of activating FcR on effector cells. Binding of the Fc portion of the antibodies to FcR leads to activation of effector cells and further release of proinflammatory cytokines and proteolytic enzymes, mediators of antibody-dependent cell-mediated cytotoxicity (ADCC). (c) Effect of antibodies and antigen-specific B cells on antigen uptake. Left panel: antigen bound by antibody is taken up via FcR on APCs such as dendritic cells or macrophages. After processing, antigen is presented on MHC molecules. This FcR-mediated antigen uptake is more efficient than antigen uptake by pinocytosis. Right panel: antigen binds to the BCR of antigen-specific B cells and is internalized. B cells are highly efficient APCs in situations of low antigen concentrations. (d) Effect of antibodies and antigen-specific B cells on antigen processing and presentation. BCR-mediated antigen uptake can influence antigen processing and the nature of MHC-displayed T-cell determinants. Likewise, antigen/antibody complexes are bound by the FcR of APCs and processed in a unique fashion dependent on the epitope specificity of the bound antibody. The BCR or antibody can shield certain protein determinants from the proteolytic attack in endocytic compartments (represented as scissors in this figure). Presentation of some determinants may thereby be suppressed, while others are boosted. Thereby cryptic pathogenic peptides may be presented and stimulate autoreactive T cells.