The Non‐H‐2 Histocompatibility Loci and Their Antigens

Graff, Ralph J.; Bailey, Donald W.

doi:10.1111/j.1600-065x.1973.tb00109.x

Cited by 37 publications

(24 citation statements)

References 37 publications

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“…Importantly, H60 immunodominance was manifested on genetically varied backgrounds with diverse sets of subordinate minor H Ags. 37 BALB.B mice differ from male B6 at an array of molecularly defined minor H Ags, including H13, H4, H7, H28, H60, and HY. Immunization of normal B6 mice with BALB.B cells results in the generation of CD8 T cells directed primarily at the immunodominant H60, H28, H4, and H7 minor H Ags.…”

Section: H60 Is a Dominant Minor H Ag In Mouse Gvhdmentioning

confidence: 99%

Real-time T-cell profiling identifies H60 as a major minor histocompatibility antigen in murine graft-versus-host disease

Choi

Christianson

Yoshimura

et al. 2002

Blood

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Section: H60 Is a Dominant Minor H Ag In Mouse Gvhdmentioning

confidence: 99%

Real-time T-cell profiling identifies H60 as a major minor histocompatibility antigen in murine graft-versus-host disease

Choi

Christianson

Yoshimura

et al. 2002

Blood

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“…The functions of minor H antigens, according to this hypothesis, would be nonimmunological in nature, unrelated to the function of the MHCo The hypothesis would explain the numerousness of minor H loci (at present there are some 40 H loci known and the existence of several hundred of these loci has been predicted, cf. [25]): the loci would serve normal, housekeeping functions in the cell and would get involved in histocompatibility phenomena only by virtue of their expression in the cell membrane.…”

mentioning

confidence: 99%

Genetics of cell-mediated lymphocytotoxicity in the mouse

Klein

1978

Springer Semin Immunopathol

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It has been said that the allograft r e a c t i o n -t h a t is, the response of host's cells to a tissue transplant from a genetically dissimilar individual of the same speciesis an artifact. Nature -so the argument goes -could not have foretold that some day surgeons and experimenters would be transplanting hearts, or kidneys, or skin in animals and man, and that there would be need to protect the integrity of the individual. Histocompatibility antigens, the cellular agents eliciting the allograft reaction, must have, therefore, some other function, perhaps totally unrelated to the allograft reaction. According to this view, the allograft reaction is worthy of studying only for practical reasons (to find ways of avoiding it), but is of little value for understanding the physiological function of histocompatibility antigens. However, recent developments in immunology, starting with the discovery of the MHC-restriction phenomenon by Zinkernagel and Doherty [60], have proved this view to be wrong, as far as antigens controlled by the major histocompatibility complex (MHC) are concerned. It appears now that the individual's own M H C molecules become alloantigens when associated with certain foreign molecules, and as such trigger a response that is indistinguishable from the classical allograft reaction. The reaction to an allogeneic tissue transplant is thus only a special case of the allograft reaction in the broadest sense. From this point of view, understanding of the allograft reaction's mechanism becomes of great theoretical importance for grasping the meaning of one of the most basic immunological phenomena.The first step in an attempt to understand the workings of the allograft reaction must be the precise definition of the genetic loci involved in the reaction. It has been toward this goal that much effort has been devoted in my laboratory, using both in vivo and in vitro models. The results of the studies using the in vitro models are briefly summarized in this communication.

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“…Several studies (23,24) indicated that the polymorphism of murine minor histocompatibility antigens is very limited. In the present study, the killing patterns of a panel of cells by the eight CTL clones revealed that hmHA-1 was expressed on five out of five cells expressing HLA-B35, and hmHA-2 and hmHA-3 were expressed on three out of four cells with HLA-B38.…”

Section: Resultsmentioning

confidence: 99%

Presentation of human minor histocompatibility antigens by HLA-B35 and HLA-B38 molecules.

Yamamoto

Kariyone

Akiyama

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

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Cytotoxic T lymphocyte (CTL) clones specific for human minor histocompatibility antigens (hmHAs) were produced from a patient who had been grafted with the kidneys from his mother and two HLA-identical sisters. Of eight CTL clones generated, four recognized an hmHA (hmHA-1) expressed on cells from the mother and sister 3 (second donor); two recognized another antigen (hmHA-2) on cells from the father, sister 2 (third donor), and sister 3; and the remaining two clones recognized still another antigen (hmHA-3) on cells from the father and sister 3. Panel studies revealed that CTL recognition of hmHA-1 was restricted by HLA-B35 and that of hmHA-2 and hmHA-3 was restricted by HLA-B38. The HLA-B35 restriction of the hmHA-1-specific CTL clones was substantiated by the fact that they killed HLA-A null/HLA-B null CTLs (3,[9][10][11][12]. Other hmHAs were also detected by CTLs (2, 4-8). As in the mouse, responses of these CTLs were restricted by major histocompatibility complex class I antigens. Only a limited number of HLA allospecificities have been reported as restriction molecules in the recognition of hmHAs. Among them, HLA-A2 and -B7 were two major ones, although there are examples of restriction by 13). These studies strongly suggested that certain HLA-A/B molecules can present hmHAs to T cells.In the present study, we attempted to generate CTL clones recognizing hmHAs from a recipient of multiple renal grafts and to characterize in detail CTL clones and corresponding hmHAs. Furthermore, the restriction elements in the CTL recognition of hmHAs were investigated by using Hmy2CIR cells transfected with HLA class I genes.MATERIALS AND METHODS Cells. B cells from the patient and the second donor (sister 3; S3 in Fig. 1) were transformed by Epstein-Barr virus (EBV). These transformed B-cell lines were grown in RPMI 1640 medium supplemented with 2 mM L-glutamine and 10% (vol/vol) fetal calf serum. EBV-transformed cell lines HVB-B5, LeolO, FS, CRB-087B, JBUSH, and AMAI were kindly supplied by F. Otani (Kitasato University, Kanagawa, Japan) and grown in the same medium. Peripheral blood lymphocytes (PBL) from six healthy staff members (Sug, YO, KT, YK, ST, and Tm) as well as those from the father, mother, sister 2 (S2), and S3 of the patient were stimulated twice by 0.2% phytohemagglutinin (PHA; Difco). The PHA-induced T cells were used as target cells for the CTL assay.Hmy2CIR cells expressing HLA-B35, -B51, or -Bw52 antigens or HLA-B51/35 chimeric antigens were previously generated (14-16). The HLA-Bw53 genomic gene has been cloned and transfected into Hmy2CIR cells (unpublished data). These cells were grown in the same medium supplemented with hygromycin B (0.2 mg/ml). Untransfected Hmy2CIR cells were grown in the medium without hygromycin B.Antibodies. W6/32 (17) and ME40.5 (18) HLA class I monomorphic, L243 HLA-DR monomorphic (19), antiLeu-10 HLA-DQ monomorphic (20), B7/21 HLA-DP monomorphic (21), OKT3 anti-human CD3 (22), OKT8 anti-human CD8 (22), OKT4 anti-human CD4 (22), and WT31 anti-human a,,3 T-cell re...

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The Non‐H‐2 Histocompatibility Loci and Their Antigens

Cited by 37 publications

References 37 publications

Real-time T-cell profiling identifies H60 as a major minor histocompatibility antigen in murine graft-versus-host disease

Real-time T-cell profiling identifies H60 as a major minor histocompatibility antigen in murine graft-versus-host disease

Genetics of cell-mediated lymphocytotoxicity in the mouse

Presentation of human minor histocompatibility antigens by HLA-B35 and HLA-B38 molecules.

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