Engagement of the B lymphocyte antigen receptor induces presentation of intrinsic immunoglobulin peptides on major histocompatibility complex class II molecules
Engagement of the B lymphocyte antigen receptor induces presentation of intrinsic immunoglobulin peptides on major histocompatibility complex class II molecules
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DOI：
10.1002/eji.1830270512
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发表时间：
1997-03-01
影响因子：
5.4
通讯作者：
Hannestad, K
中科院分区：
文献类型：
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作者：
Bartnes, K;Hannestad, K
通过克隆型可变区，免疫球蛋白(Ig)是B细胞肿瘤的肿瘤特异性抗原。我们报道，B细胞抗原受体(BCR)的结合促进来自B细胞固有Ig的多肽呈递到主要组织相容性复合体(MHC)II类限制性T细胞。因此，抗Ig赋予来自H-2(D)、Ig恒定重链同种异型b(IGC(H)(B))小鼠的正常体外B淋巴细胞刺激I-A(D)限制性T细胞克隆的能力，该克隆识别伽马2a(B)435-451别肽。相应的自身伽马2a(A)肽是隐蔽的，抗原性比伽马2a(B)别肽少6000倍。尽管如此，表达表面(S)IgG2a(A)的同基因B细胞淋巴瘤A20也被BCR结扎后的T细胞识别。因此，抗Ig引发了一种隐蔽的肿瘤抗原决定簇的披露。我们认为，自身抗原通过结合自身反应性B细胞的BCR，诱导产生T辅助细胞(Th)不耐受的内源性Ig多肽。这样，具有抗自身潜能的B细胞就可以在不识别标称自身抗原的情况下被激活。
By means of the clonotypic variable region, the immunoglobulin (Ig) is a tumor-specific antigen on B cell neoplasms. We report that engagement of the B cell antigen receptor (BcR) promotes presentation of peptides derived from the B cell's intrinsic Ig to major histocompatibility complex (MHC) class II-restricted T cells. Thus, anti-Ig endowed normal, ex vivo B lymphocytes from H-2(d), Ig constant heavy chain allotype b (IgC(H)(b)) mice with the capacity to stimulate an I-A(d)-restricted T cell clone which recognizes the gamma 2a(b) 435-451 allopeptide. The corresponding self gamma 2a(a) peptide is cryptic and 6000-fold less antigenic than the gamma 2a(b) allopeptide. Even so, the syngeneic B cell lymphoma A20 which expresses surface (s) IgG2a(a), was also recognized by the T cells after BcR ligation. Thus, anti-Ig triggered the disclosure of a cryptic tumor antigen determinant. We propose that autoantigens, by engaging the BcR of self-reactive B cells, induce presentation of intrinsic Ig peptides to which the T helper cell (Th) repertoire is not tolerant. In this way, B cells with anti-self potential may be activated without Th recognition of nominal autoantigen.