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PubMed1981

A new minor histocompatibility locus linked to H-3.

B10, BALB.B, and A.BY shared an allele at a new locus not shared by B10.LP-H-3b. This locus is linked to the minor histocompatibility gene, H-3, in the 5th linkage group of chromosome 2 of the mouse. The product of the new gene fits the criteria of a minor histocompatibility antigen, since it induced as well as served as a target for cytotoxic lymphocytes (CTL) and its presence accelerated skin graft rejection when compared with that caused by H-3.1. F1 complementation of skin graft rejection and generation of CTL indicated that A.BY and BALB.B do not share H-3a with B10 as previously reported but possess the c allele of their congenic partners A and BALB/c. Thus, B10.LP-H-3b and B10 differ from one another by at least 2 minor histocompatibility loci. The specificity of CTL developed in B10. LP-H-3b and appropriate F1 hybrids indicate that the lytic activity of CTL specific for H-3.1 was restricted to target cells possessing H-2Kb antigens; this contrasted to the H-2Db-restricted activity of CTL specific for the product of the new gene.

Animals↗

PubMed1980

Partial N-terminal amino acid sequences of guinea pig classic histocompatibility antigens.

Partial N-terminal amino acid sequences were determined by microsequencing for three of the guinea pig GPLA-B classic histocompatibility antigens, which are presumably allelic products. The sequences of GPLA-B.1 derived from the noncongenic inbred strain 2 and strain 13 animals showed no differences a their N-termini, suggesting that these molecules are chemically as well as serologically identical. Two residues, isoleucine and leucine, were found at position 5 of the sequence of GPLA-B.1, suggesting that GPLA-S, the product of the second classic histocompatibility locus, was being cosequenced. GPLA-B.2 and GPLA-B.3 antigens showed distinct sequence differences from GPLA-B.1 and from each other. The sequences of GPLA-B.3 derived from a random-bred guinea pig and from the inbred DHCBA strain showed no differences and showed a possible species specific residue. All sequences showed significant homology with histocompatibility antigens of other species, suggesting a common evolutionary origin.

Amino Acid Sequence↗

PubMed1993

Differential binding of a minor histocompatibility antigen peptide to H-2 class I molecules correlates with immune responsiveness.

Minor histocompatibility (H) Ag are recognized in the context of MHC class I (K/D) molecules and can constitute a strong barrier to tissue transplantation. The products encoded by the MHC (H-2 in mice) have been shown recently to be Ag-presenting molecules that bind foreign and self peptides in their peptide binding sites. Different class I molecules preferentially bind different arrays of endogenous peptides for presentation to CTL. Previous studies showed that the Kb-restricted CTL response to one minor histocompatibility Ag, H-4, varied in different Kb mutants. One possible basis for this variation might be that the response is regulated by the level of binding of an H-4 peptide by class I molecules. To analyze this possibility, we initiated studies to identify the H-4 peptide that is included in the array of self peptides. The complete mixture of peptides eluted from Kb molecules of H-4+ tumor cells was able to sensitize H-4- targets for lysis by H-4-specific CTL. The presence of a specific H-4 peptide was confirmed when the radiolabeled peptide mix eluted from Kb molecules was separated by HPLC. Only one peak in the profile of H-4+ tumor peptides was capable of sensitizing H-4- targets for lysis by H-4-specific CTL; this active peak was absent in H-4 mutant cells. Peptide mixtures eluted from a panel of Kb mutant molecules extracted from H-4+ lymphocytes varied in their capacities to sensitize targets for H-4-specific lysis and the relative sensitization correlated with the demonstrated capacity of mutant mice to generate H-4-specific CTL. Therefore, the highly specific genetic control of the T cell response to the H-4 minor histocompatibility Ag appears to be due to the differential binding of an H-4 peptide by class I molecules.

Animals↗

PubMed1975

H-2-linked genetic control of resistance to histocompatible tumors.

The role of the major histocompatibility complex of the mouse (H-2) in resistance to two transplanted histocompatible tumors was evaluated by determining the differences in survival times between the syngeneic parent strain and various F1 hybrids. C57BL/10nSn (B10) mice and their F1 hybrids were given injections of a methylcholanthrene-induced fibrosarcoma of B10 origin. The B10 x B10.BR F1, B10 x B10.M F1, B10 x B10.WB F1, and B10 x 5R F1 hybrids survived significantly longer than the B10 parental strain or B10 x B10.D2 F1 and B10 x 18R F1 animals, while B10 x 2R F1 mice succumbed significantly sooner than any of the above groups. Statistical comparisons of geometric mean survival times of the strain of tumor origin (B10) versus the F1 hybrids showed the influence of genes coded for the H-2 complex in the phenomenon, termed "hybrid resistance" or "allogeneic inhibition." However, tumor resistance did not occur in all hybrids and could not be attributed to a single dominant Ir gene localized in the I region as might be predicted if the phenomenon involved genetic control of immunological responsiveness to tumor-specific transplantation antigens. Similarly, in a second group of experiments, the mean survival times of DBA/2 x B10.D2 F1 animals given injections of the 815 mastocytoma of DBA/2(D2) origin was compared to the mean survival times of various hybrids with the D2 parent. Again, the results demonstrated the importance of the H-2 gene complex in this phenomenon. However, the above results did not permit precise localization of the H-2-linked gene(s) responsible for differential resistance to the histocompatible tumor.

Animals↗

PubMed1993

Endothelial activation by hydrogen peroxide. Selective increases of intercellular adhesion molecule-1 and major histocompatibility complex class I.

Products of activated leukocytes may alter vascular endothelial cell (EC) function. For example, ECs respond to leukocyte-derived cytokines, such as tumor necrosis factor (TNF) or interleukin-1, by reversibly altering levels of expression of specific gene products that promote inflammation. In contrast, hydrogen peroxide, a product of TNF-activated neutrophils, can produce irreversible EC injury and death. In this study, we have investigated the effects of subinjurious concentrations of hydrogen peroxide on EC inflammatory functions. Treatment with 50 to 100 mumol/L hydrogen peroxide selectively increases surface expression of intercellular adhesion molecule-1 and major histocompatibility complex class I, but not endothelial leukocyte adhesion molecule-1 (also known as E-selectin), vascular cell adhesion molecule-1, or gp96, a constitutively expressed EC surface protein. Increased major histocompatibility complex class I and intercellular adhesion molecule-1 surface expression is associated with specifically increased messenger RNA levels, suggesting selective endothelial gene activation. Hydrogen peroxide does not activate the transcription factor Nuclear Factor kappa B, an important mediator of TNF-induced gene expression. Co-treatment with hydrogen peroxide inhibits TNF-induced gene expression at 4 hours, an effect which can be attributed to reversible inhibition of TNF binding to EC surface receptors. Hydrogen peroxide also antagonizes the actions of interleukin-1. At 24 hours, TNF and hydrogen peroxide produce, at most, additive increases in intercellular adhesion molecule-1 and major histocompatibility complex class I. These results suggest that subinjurious concentrations of hydrogen peroxide can activate endothelium and that the effects of hydrogen peroxide on ECs differ from those of inflammatory cytokines.

Antigens, Surface↗

PubMed1994

Combination of cyclosporine and splenectomy suppresses interleukin-6 production and major histocompatibility complex class II expression and prolongs cardiac xenograft survival.

Although untreated Lewis rat recipients will reject a transplanted hamster heart in 3 days, accommodation of heart xenografts can be induced by treatment with cyclosporine and splenectomy, improving graft survival to greater than 50 days. Both humoral and cellular arms of the immune system may be involved in the mechanisms responsible for the prolongation of graft survival. Our objective was to study the impact of cyclosporine and splenectomy on the deposition of antibodies, complement, or both within the graft. We also compared the cellular component of inflammation in treated recipients with that in untreated controls. Inbred male Lewis rats given cyclosporine 15 mg/kg per day were splenectomized 2 days after they had received heterotopic heart transplants from Golden Syrian hamsters. Recipients of syngeneic grafts or untreated xenografts served as controls. Plasma interleukin-6 activity was measured in a standard proliferation assay with 7TD1 hybridoma cells. Deposition of immunoglobulin M, immunoglobulin G, and complement in heart tissue was evaluated by immunofluorescence. Cells infiltrating the graft that expressed major histocompatibility complex class II antigens were identified by immunohistochemical staining with OX6 antibodies. In xenograft recipients receiving immunosuppression, interleukin-6 activity, immunoglobulin M and complement deposition were significantly reduced, graft infiltration was mild, and cardiac function was good compared with the results in those without treatment 3 and 10 days after implantation. Inflammatory cells expressing major histocompatibility complex class II antigens were significantly reduced in immunosuppressed xenograft recipients (2.8 +/- 0.4 cells/high power field) compared with those in xenogeneic controls (9.5 +/- 0.6 cells/high power field; p < 0.0005). The significant decrease in deposition of humoral components (immunoglobulin M and complement), interleukin-6 plasma levels, and expression of major histocompatibility complex class II antigens by inflammatory cells within the nonrejecting grafts suggests that the synergistic benefit of cyclosporine and splenectomy depends on the attenuation of both cellular and humoral mechanisms of xenograft rejection.

Animals↗

PubMed1988

Elevated mRNA levels of major histocompatibility complex class II genes in lymphocytes of autoimmune BB rats.

The BB rat spontaneously develops autoimmune abnormalities such as insulin-dependent diabetes mellitus and thyroiditis. The autoimmunity of the BB rat is controlled in part by genes of the major histocompatibility complex (MHC), known as the RT1 complex in the rat, and accumulating evidence suggests the involvement of MHC class II molecules. The RT1 complex specifies two types of class II molecules, which are encoded by the loci RT1.B and RT1.D. We have determined the relative steady-state mRNA levels of the class II genes RT1.B beta, RT1.D alpha, and RT1.D beta in splenic lymphocytes from individual autoimmune BB rats of various ages and from age-matched histocompatible normal Wistar-Furth (WF) rats. The relative steady-state mRNA levels of the RT1.D alpha and RT1.D beta genes, but not of the RT1.B beta gene, were elevated approximately 2.5-fold in lymphocytes of prediabetic BB rats 45-75 days old in comparison with age-matched normal WF rats and older BB rats greater than 75 days old. In the diabetic and nondiabetic BB rats greater than 75 days old, the RT1.D alpha and RT1.D beta transcripts were found at lower normal levels, similar to that of WF rats. In contrast, the RT1.B beta transcripts were found at comparable levels in lymphocytes of the BB and WF rats at all ages examined. The increased steady-state mRNA levels of the RT1.D alpha and RT1.D beta genes in the prediabetic BB rats may reflect differences in the proportion of lymphocytes expressing these genes and thus differences in splenic lymphocyte populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effect of mismatches for major histocompatibility complex and minor antigens on corneal graft rejection.

The importance of minor histocompatibility genes in corneal graft rejection was investigated using a model that simulates the major histocompatibility complex (MHC) and minor mismatches of the human allograft more accurately than previous animal models. DA(RT1a) x LEW(RT1(1]F1 hybrid rats were backcrossed to LEW, and the backcross generation were used as corneal graft recipients. Female DA(RT1a) strain animals were used as donors throughout. As in humans, the MHC disparity (a to 1) between each donor-recipient pair could be controlled; minor mismatches were variable and unknown. The MHC haplotype of each backcross individual (either homozygous l/l) or heterozygous a/l) was determined. Depending on this haplotype, the transplanted DA cornea was either matched or mismatched with the recipient for MHC antigens. The average proportion of minor disparate loci was 50%, although this was variable and unknown from recipient to recipient. Some animals of each MHC type were sensitized with three subcutaneous DA strain skin grafts at intervals of 2 weeks. Prior sensitization caused more rapid corneal graft rejection in both MHC mismatched (P less than 0.001) and matched (P less than 0.01) animals. All animals in the two MHC-mismatched groups (sensitized, 26; unsensitized, 17) and most in the MHC-matched groups (sensitized, 25 of 27; unsensitized, all 13) rejected their grafts. The MHC matching resulted in a greater range of survival times, although the difference in survival in unsensitized animals between matched and mismatched groups was not significant (unsensitized, P greater than 0.05; sensitized, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Major histocompatibility complex of the mole-rat. II. Restriction fragment polymorphism.

The major histocompatibility complex (Mhc) is a group of loci coding for lymphocyte membrane glycoproteins that provide the context for the recognition of foreign antigens in the initial phase of the immune response. The complex contains a large number of loci, some of which are highly polymorphic. The complexity and polymorphism pose a number of questions concerning the evolution of the Mhc. In an attempt to answer some of these questions, we have begun to study the Mhc of the mole-rat, Spalax ehrenbergi, a rodent representing a complex of sibling species occupying ecologically and geographically clearly delineated regions within the borders of Israel. In an earlier publication we identified the Spalax major histocompatibility (Smh) complex serologically and biochemically. Here, we analyze the Smh by Southern blotting of DNA fragments produced by restriction enzyme digestion. The fragments were hybridized to mouse probes specific for class I, class II, and C4 genes. The analysis has revealed that the Smh complex contains as many class I genes as the mouse does and that these genes are polymorphic. The number of class II genes could not be determined with certainty, but it is probably not greater than in the mouse. Polymorphism was also detected at the loci coding for the complement component 4 (C4), which are probably closely linked to the Smh complex. The polymorphism of mole-rat class I loci contrasts with the reported monomorphism of these loci in the Syrian hamster. Since the mole-rat leads a solitary, subterranean life, as the Syrian hamster does, ecology cannot be an explanation for the lack of class I polymorphism in the latter species.

Animals↗

PubMed1991

Uneven tissue distribution of minor histocompatibility proteins versus peptides is caused by MHC expression.

Naturally processed minor histocompatibility (H) peptides corresponding to H-4b, H-Y, and an unmapped BALB.B minor H gene were quantified in a relative way in 15 different tissues of male BALB.B mice. For one of these minor H antigens, we could also determine the relative content of the respective protein. For each minor H peptide, an individual tissue distribution was found. Tissues expressing little or no MHC (major histocompatibility complex), like brain, contained only small amounts of minor H peptides or none at all, although the same tissues contained minor H protein in substantial quantities. By contrast, Kb-expressing brains from mice transgenic for Kb under control of the glial acidic protein promoter contained both minor H peptide and protein in high amounts. Thus, the expression of minor H peptides in a given tissue is dependent on coexpression of the restricting MHC class I molecules.

Animals↗

PubMed2006

Conserved extended haplotypes of the major histocompatibility complex: further characterization.

Since the complete sequencing of a human major histocompatibility complex (MHC) haplotype, interest in non-human leucocyte antigen (HLA) genes encoded in the MHC has been growing. Non-HLA genes, which outnumber the HLA genes, may contribute to or account for HLA and disease associations. Most information on non-HLA genes has been obtained in separate studies of individual loci. To comprehensively address polymorphisms of relevant non-HLA genes in 'conserved extended haplotypes' (CEH), we investigated 101 International Histocompatibility Workshop reference cell lines and nine additional anonymous samples representing all 37 unambiguously characterized CEHs at MICA, NFKBIL1, LTA, NCR3, AIF1, HSPA1A, HSPA1B, BF, NOTCH4 and a single nucleotide polymorphism (SNP) at HLA-DQA1 as well as MICA, NOTCH4, HSPA1B and all five tumour necrosis factor short tandem repeat (STR) polymorphisms. This work (1) provides an extensive catalogue of MHC polymorphisms in all CEHs, (2) unravels interrelationships between HLA and non-HLA haplotypical lineages, (3) resolves reported typing ambiguities and (4) describes haplospecific markers for a number of CEHs. Analysis also identified a DQA1 SNP and segments containing MHC class III polymorphisms that corresponded with class II (DRB3 and DRB4) lineages. These results portray the MHC where lineages containing non-HLA and HLA variants in linkage disequilibrium may operate in concert and can guide more thorough design and interpretation of HLA-disease relationships.

3' Untranslated Regions↗

PubMed1991

Expression of CD4 in transgenic mice alters the specificity of CD8 cells for allogeneic major histocompatibility complex.

We have generated a transgenic mouse line in which a CD4 transgene is expressed on a significant fraction of the mature CD8+ lymphocytes but is not expressed in the thymus. This provides an opportunity to examine the functional consequences of CD4 expression in a population of class I-selected CD8+ lymphocytes. CD8+ lymphocytes expressing the CD4 transgene proliferate in response to allogeneic class I and class II major histocompatibility complex, whereas CD8+ cells from control animals proliferate only to allogeneic class I gene products. These observations suggest that the ability of a T-cell population to react with class II allogeneic major histocompatibility complex is determined by the presence of CD4.

Animals↗

PubMed1991

Growth inhibition of clonogenic leukemic precursor cells by minor histocompatibility antigen-specific cytotoxic T lymphocytes.

Minor histocompatibility (mH) antigens appear to play a major role in bone marrow transplantation (BMT) using HLA-identical donors. Previously, we reported the isolation of major histocompatibility complex (MHC)-restricted mH antigen-specific cytotoxic T lymphocytes (CTL) from patients with graft-vs.-host disease or rejection after HLA-identical BMT. We have demonstrated that mH antigens can be recognized on hematopoietic progenitor cells, and residual recipient CTL specific for mH antigens expressed on donor hematopoietic progenitor cells may be responsible for graft rejection in spite of intensive conditioning regimens in HLA-identical BMT. Here, we investigated whether mH antigen-specific CTL directed against the mH antigens HA-1 to HA-5 and the male-specific antigen H-Y were capable of antigen-specific inhibition of in vitro growth of clonogenic leukemic precursor cells. We demonstrate that mH antigen-specific CTL against all mH antigens tested can lyse freshly obtained myeloid leukemic cells, that these mH antigen-specific CTL can inhibit their clonogenic leukemic growth in vitro, and that this recognition is MHC restricted. We illustrate that leukemic (precursor) cells can escape elimination by mH antigen-specific CTL by impaired expression of the relevant MHC restriction molecule. We suggest that mH antigen-specific MHC-restricted CTL may be involved in vivo in the graft-vs.-leukemia reactivity after BMT.

Acute Disease↗

PubMed2003

An immunodominant minor histocompatibility alloantigen that initiates corneal allograft rejection.

BACKGROUND: Murine orthotopic corneal allografts experience immune privilege and have good survival as compared with skin allografts. However, privilege is not complete, and some grafts are still rejected. Unexpectedly, corneas expressing minor histocompatibility (H) alloantigens are rejected at a higher rate than major histocompatibility complex (MHC) disparate grafts. We hypothesize that certain immunodominant minor H alloantigens are extremely immunogenic when expressed in corneal tissue, terminate ocular immune privilege, and initiate corneal allograft rejection. METHODS AND RESULTS: Corneal allograft survival and the role of CD4+ T cells and CD8+ T cells were examined in corneal transplants that expressed genetically defined minor H3 alloantigens. The H3 locus contains at least two minor H genes. H3a is presented by MHC class I and recognized exclusively by CD8+ T cells. H3b is presented by class II and recognized exclusively by CD4+ T cells. Congenic strains that differ from C57BL/10 at (1) H3a, (2) H3b, or (3) H3a+H3b were used for orthotopic corneal and skin transplants. Donor corneas expressing either H3a or H3a+H3b experienced immune privilege and survived longer than skin allografts. By contrast, donor corneas expressing H3b (recognized by CD4+ T cells) experienced vigorous rejection and were eliminated faster than skin allografts. CONCLUSION: There are minor H alloantigens that terminate ocular immune privilege and initiate corneal allograft rejection. These minor H alloantigens are more immunogenic when expressed in corneal tissue than when they are expressed in skin allografts.

Animals↗

PubMed1981

The major histocompatibility complex of primates: evolutionary aspects and comparative histogenetics.

All mammalian species investigated have a chromosomal region designated as the major histocompatibility complex or m.h.c. The biological significance of the m.h.c. goes far beyond controlling the most important histocompatibility or transplantation antigens; the capacity to respond immunologically, the susceptibility to disease (including cancer), the serum level of several complement factors and numerous other biological traits are regulated by genetic systems closely linked within that chromosomal region. While the basic structure of the m.h.c. seems to be rather similar for all mammalian species, the similarities among the m.h.c. of human and non-human primates are particularly impressive. In this communication, m.h.c. gene products of rhesus monkey, chimpanzee and man are compared and reviewed. Evolutionary aspects of the persistence of the m.h.c. region or 'supergene' throughout the animal kingdom are discussed.

Animals↗

PubMed1991

Major histocompatibility complex antigen expression on lymphocytes from aging strain A mice.

Molecules encoded by the major histocompatibility complex (MHC) are crucial for the proper functioning of the immune response. In this study, the levels of class I and class II major histocompatibility antigens on lymphocytes from strain A mice were measured as a function of age. Class I protein levels increased significantly on both peripheral blood and spleen (T cells and B cells) lymphocytes with age. This increase in MHC class I protein levels was accompanied by an increase in class I mRNA levels. On the other hand, class II protein levels did not show a significant change with age. Moreover, while the percentage of class I-expressing spleen lymphocytes stayed at a steady-state level of 100% with age, the percentage of class II-expressing spleen lymphocytes decreased from 85% in young animals to 70% in old animals. This decrease was due to a decrease in the relative proportion of B cells compared to T cells in the spleen lymphocyte population of old mice. When class II mRNA levels were measured, it was found that these levels decreased markedly with age. Overall, it is clear that the regulation of MHC class I and class II expression changes with age in A strain mice. Since optimal levels of MHC expression are crucial for the proper functioning of cellular and humoral immune responses, it will be most interesting to understand how the control of MHC gene expression changes with age and whether MHC gene expression can be modulated in old individuals to restore better immune function.

Aging↗

PubMed1988

Genetic and stimulator cell requirements for generation and activation of minor histocompatibility antigen-specific memory cytotoxic T-lymphocyte precursors.

By adding IL-2 (supernatant of culture of concanavalin A-activated rat spleen cells) on Day 3 of mixed leucocyte cultures (MLC) we managed to fully activate multiple minor histocompatibility antigen (MIHA)-specific cytotoxic T-lymphocyte precursors (CTLp). In this newly developed system we studied genetic and stimulator cell requirements for the generation and activation of MIHA-specific memory CTLp. Memory CTLp were activated to generate effector CTL in MLC only when major histocompatibility complex (MHC)-compatible MIHA-allogeneic cells were used as stimulators. In contrast, memory CTLp were generated in mice that were primed by injection of either MHC-compatible or incompatible MIHA-allogeneic spleen cells. A surprisingly small number (10(4] of MHC-disparate cells cross-primed mice effectively. For priming, no special accessory cell types were required as stimulators, and 10(4) adherent cell-depleted spleen cells primed mice as well. These results contrasted to another finding that sonication-disrupted 10(6) stimulator cells did not prime mice effectively, and antigens shed from 10(7) live stimulator cells failed to sensitize host antigen-presenting cells for priming. It is suggested from these results that the mode of recognition of MIHA by virgin CTLp is unique or that an as yet unknown unusual stimulation pathway works for the priming.

Animals↗

PubMed1996

Generation of in vitro natural cytotoxicity of horse lymphocytes against sarcoid-derived tumor cells not expressing major histocompatibility complex antigens.

OBJECTIVE: To analyze in vitro lymphocyte-mediated immune responses of horses with sarcoids against allogeneic sarcoid cells containing endogenous retrovirus but not expressing major histocompatibility complex antigens. DESIGN: Lymphocyte-mediated immune reactions were assessed by means of proliferative responses in mixed lymphocyte tumor cell culture (MLTC) assay and lymphocyte-mediated cytotoxicity against various equine target cells. ANIMALS: 12 horses with sarcoid tumors and 15 control horses. PROCEDURE: Blood lymphocytes were cocultured in MLTC with allogeneic sarcoid cells (Mc-1, BayMc-1), equine testis cells, or normal equine dermal fibroblasts. Lymphocytes were assayed for proliferative responses by [3H]thymidine uptake and for cytotoxicity against the same targets by 51Cr release assay. The lymphocyte populations were analyzed for some common surface markers. RESULTS: Lymphocytes from horses with sarcoids exerted an anamnestic proliferative response in MLTC against Mc-1 cells, but this procedure never generated cytotoxic lymphocytes. However, lymphocytes from all horses cultured in medium with 10% allogeneic serum only had selective. natural cytotoxicity against Mc-1 that was generated without DNA synthesis. Approximately 80% of the lymphocytes disappeared during culture; however the remaining population of small, viable lymphocytes indicated a decrease of CD4+ T lymphocytes, but numbers of T cells with receptors for Helix pomatia A hemagglutinin were unaffected. Few lymphocytes had Fc-receptors for IgG, were complement-reactive positive cells or were B cells expressing surface immunoglobulin. CONCLUSIONS: Results may indicate a natural defense system, which preferentially recognizes and lyses tumor cells that are deficient in surface expression of major histocompatibility complex antigens, without intervention of conventional T-cell receptors or antibodies.

Animals↗