Carreno B M, Anderson R W, Coligan J E, Biddison W E
Molecular Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Proc Natl Acad Sci U S A. 1990 May;87(9):3420-4. doi: 10.1073/pnas.87.9.3420.
T-cell recognition of peptides that are bound and presented by class I major histocompatibility complex molecules is highly specific. At present it is unclear what role class I peptide binding plays relative to T-cell receptor specificity in determination of immune recognition. A previous study from our group demonstrated that the HLA-A2.1 molecule could bind to 25% of the members of a panel of unrelated synthetic peptides as assessed by a functional peptide competition assay. To determine the peptide-binding specificity of another HLA class I molecule, we have examined the capacity of this panel of peptides to compete for the presentation of influenza virus nucleoprotein peptide NP-(335-350) by HLA-B37 to NP-peptide-specific HLA-B37-restricted cytotoxic T-lymphocyte lines. Forty-two percent of peptides tested were capable of inhibiting NP-(335-350) presentation by HLA-B37. Remarkably, none of these HLA-B37-binding peptides belong to the subset that was previously shown to bind to the HLA-A2.1 molecule. Only the NP-(335-350) peptide was capable of binding to both HLA-A2.1 and HLA-B37. These findings demonstrate that the peptide-binding specificities of HLA-B37 and HLA-A2.1 are largely nonoverlapping and suggest that, from the universe of peptides, individual HLA class I molecules can bind to clearly distinct subsets of these peptides.
T细胞对由I类主要组织相容性复合体分子结合并呈递的肽段的识别具有高度特异性。目前尚不清楚在免疫识别的决定过程中,I类肽段结合相对于T细胞受体特异性发挥何种作用。我们小组之前的一项研究表明,通过功能性肽段竞争试验评估,HLA - A2.1分子能够与一组不相关的合成肽段中的25%结合。为了确定另一种HLA I类分子的肽段结合特异性,我们检测了这组肽段竞争HLA - B37将流感病毒核蛋白肽NP-(335 - 350)呈递给NP肽特异性的HLA - B37限制性细胞毒性T淋巴细胞系的能力。42%的测试肽段能够抑制HLA - B37对NP-(335 - 350)的呈递。值得注意的是,这些与HLA - B37结合的肽段中没有一个属于先前显示能与HLA - A2.1分子结合的亚组。只有NP-(335 - 350)肽段能够同时与HLA - A2.1和HLA - B37结合。这些发现表明,HLA - B37和HLA - A2.1的肽段结合特异性在很大程度上不重叠,这表明在整个肽段范围内,单个HLA I类分子能够结合这些肽段中明显不同的亚组。