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1.
Takashi Morita Christiane Delarbre Michel Kress Philippe Kourilsky Gabriel Gachelin 《Immunogenetics》1985,21(4):367-383
Two recombinant mice have been recovered from the progeny of Ttf/t
w32+ animals. They have lost the tw32 lethality factor(s) and gained tufted, presumably from the T chromosome. Southern blot analysis of class I genes of these two new partial t
PA027 and t
PA286 haplotypes indicates that they have retained at least part of the major histocompatibility complex of the t
w32 chromosome (H-2 haplotype H-2
w28). We have prepared a phage library of Eco RI-digested DNA from homozygous t
PA027 animals. Upon screening the library with a cDNA probe specific for H-2K genes, we isolated a class I gene displaying all of the distinctive features of a genuine H-2K gene, and which could thus be defined as an H-2K
w28 gene. The H-2K
w28 gene is 92–95% homologous to H-2K
band H-2K
dgenes and differs significantly from the other class I genes sequenced so far. Homology with the H-2K
bsequence reaches nearly 100% in the 3 part of the H-2K
w28 gene. Moreover, the homology with an H-2K
qcDNA sequence reaches 99.8%. Several hypotheses can account for the near identity of H-2K
b, H-2K
q,and H-2K
w28 gene sequences: either recombination between H-2
w28 and H-2
band H-2
qsequences occurred before or at the.time the strain was established, or the class I genes of the t
w32 chromosome and the H-2
band H-2
qgenes found in inbred strains of mice have separated from each other rather recently. 相似文献
2.
Characterization of a novel IRF-1-deficient mutant cell line 总被引:1,自引:0,他引:1
3.
Cloned B-cell lines from a female T16H/XSxr mouse in which Tdy expression was suppressed due to X inactivation and from a male X/XSxr mouse, both of the (kxb)F1 haplotype, were examined for H-Y expression. This was determined both by their ability to act as targets for H-2k and H-2b-restricted H-Y-specific cytotoxic T cells and by their ability to stimulate the proliferation of H-2Kk, H-2Db (class I) and Ab (class II)-restricted T-cell clones. In B-cell clones from the T16H/XSxr mouse, expression of H-Y/Db exhibited partial X inactivation and only a proportion ( 30%) of the cells were targets for or stimulated H-2Db-restricted H-Y-specific T cells. In contrast, H-Y eiptopes restricted by H-2k (H-Y/Kk, H-Y/Dk) and Ab (H-Y/Ab) exhibited no X inactivation. Furthermore, no inactivation of H-Y/Db, H-Y/Ab, or H-Yk was observed in the male X/XSxr mouse. These results indicate that the T16H/XSxr female is a mosaic, as a result of the variable spread of X inactivation into the Sxr region. They further suggest that the H-Y antigen recognized in association with H-2k and H-2Db class I molecules and Ab class II molecules may be the product of more than one gene. 相似文献
4.
The interaction between class I major histocompatibility complex (MHC) products and T cells was studied using H-2Kb-specific alloreactive T-cell lines and clones obtained by repeated in vitro stimulation with allogeneic cells. Induction of proliferation of these T cells appeared to involve two signals: the H-2Kb alloantigen and interleukins. Immunopurified liposome-inserted H-2Kb, which stimulates specific secondary in vitro cytotoxic T lymphocyte (CTL) responses, could not replace cell-associated H-2Kb in the stimulation of these T-cell lines, even in the presence of feeder cells and interleukins. When T-cell lines were initiated in vitro and repeatedly stimulated with H-2Kb liposomes and feeder cells, it was possible to obtain T cells that could proliferate in response to H-2Kb liposomes in the presence of feeder cells and interleukin-2-containing supernatants or on H-2K
b
-expressing cells. Only stimulation with cells permitted maintenance of these T cells in culture for more than 12 weeks. Analyses of cell surface markers and of patterns of inhibition of proliferation by monoclonal antibodies (mAb) of T-cell lines induced in vitro with cell- or liposome-associated H-2Kb indicated that T-cell stimulation by class I antigen can occur in at least two ways. In the first, the H-2Kb-induced proliferation of Lyt-1- Lyt-2+ T4- T cells is inhibited by H-2Kb- and by Lyt-2-specific mAb, but not by Ia or T4-specific mAb. In the second, both Lyt-2+ and T4+ T cells are involved and the H-2Kb-induced proliferation is inhibited by H-2Kb- and Lyt-2-specific mAb and by Ia- and T4-specific mAb.Abbreviations used in this paper Ab
antibody
- mAb
monoclonal antibody
- C
complement
- i.p.
intraperitoneally
- PBS
phosphate-buffered saline
- PBS-B-N
PBS containing bovine serum albumin and NaN3
- CTL
cytotoxic T lymphocyte
- Th
T helper cell
- MHC
major histocompatibility complex
- PMA
4-phorbol 12-myristate 13-acetate
- SCA
concanavalin A-stimulated rat spleen cell supernatant
- SC16
EL4 clone 16 supernatant
- IL-1
interleukin-1
- IL-2
interleukin-2 (T-cell growth factor)
- FCS
fetal calf serum
- H-2Kb-lip.
H-2Kb inserted in liposomes
- C. E.
cell equivalents 相似文献
5.
Mayumi Nakagawa Richard A. Zeff Steven S. Geier Jeffrey A. Bluestone Stanley G. Nathenson 《Immunogenetics》1986,24(6):381-385
A cell-surface-associated variant H-2K product was expressed by an Abelson virus-induced pre-B-cell line after chemical mutagenesis with ethyl methane sulfonate. The variant cell line (R8.313) was previously demonstrated to have altered allodeterminants in Kb as demonstrated by both Kb-specific monoclonal antibody binding and alloreactive cytotoxic T lymphocyte (CTL) cytolysis. The mutant H-2K
b gene from R8.313 was cloned and characterized in detail. DNA sequence analysis of the region of the gene corresponding to the three extracellular domains identified a single point mutation resulting in a leucine-to-phenylalanine substitution at amino acid residue 82. The site of mutation within the 1 domain was confirmed by oligonucleotide hybridization analysis. Mouse L-cell fibroblasts transfected with the mutant gene were recognized with the same monoclonal antibody binding and CTL lytic pattern as the R8.313 cell line, confirming that the altered phenotype of the mutant cell line was due to a point mutation in the H-2K
b gene. These data further extend the hypothesis that the region of amino acid residues 70–90 in the 1 domain is important in the formation of both antibody and CTL-defined recognition structures on major histocompatibility complex class I molecules. 相似文献
6.
Functional studies concerning the unique interaction between class I H-2 allodeterminants and cytolytic T lymphocyte (CTL) antigen receptors have benefitted from the development of H-2Kb mutant mouse strains and somatic H-2 variants selected with monoclonal antibody. Here, we describe the development of a novel approach to immunoselection of somatic H-2Kb variants employing a Kb-specific CTL clone as the negative selective agent. The rationale for this method is that the use of an alloreactive CTL clone as the selective agent should enable us to detect the emergence of structural Kb variants based on their loss of the relevant CTL-defined allodeterminant. Thus, these structural variants are well suited to an in-depth analysis of the functional relationship between H-2 antigens and receptor recognition by CTL. Using this approach, we successfully isolated two types of structural Kb variants, as well as numerous Kb-loss variants. The functional studies described in this paper indicate that these structural variants exhibit alterations in expression of both CTL-defined and serologically defined H-2Kb allodeterminants. The structural characterization of such variants should enable us to identify the precise amino acid residues responsible for the creation of the relevant CTL-defined Kb allodeterminants. 相似文献
7.
Lin-Na Ding Ken-ichi Isobe Tomoaki Yoshida Kohei Kawashima Izumi Nakashima 《Cancer immunology, immunotherapy : CII》1990,31(2):115-120
Summary The recombinant H-2Kb-erbB gene, encoding for a part of the H-2 class I antigen and the kinase domain of the V-erbB peptide, was successfully introduced into murine mastocytoma P815 variant P1.HTR cells, which resulted in low but significant cell-surface expression of the hybrid gene product. When the chimeric gene transfectant was inoculated into the CDF1 mice, it soon grew but regressed thereafter. The tumorigenicity of this transfectant was lower than the H-2Kb gene transfectant that expressed the H-2Kb antigen at a comparable level. These CDF1 mice that had received the chimeric gene transfectant obtained a high-grade anti-tumor immunity against the challenge of a high dose of parental tumor. Corresponding to these observations, anti-tumor cytotoxic T lymphocytes, which lyse parental P1.HTR cells but not syngeneic L1210 or NS-1 tumor cells, were developed in the peritoneal cavity of mice that had been inoculated with the transfectant and parental tumor. Definite antibody activity binding to parental P1.HTR tumor cells was also demonstrated in the sera of these mice, precipitating 40-kDa, 74-kDa and 98-kDa molecules from the surface of the radiolabeled P1-HTR tumor cells. The results suggested that the chimeric H-2-erbB gene transfectant efficiently triggers both cellular and humoral anti-tumor immune responses. 相似文献
8.
Weisong Xu Edwin de Zoeten Victoria Carr-Brendel E. P. Cohen 《Cancer immunology, immunotherapy : CII》1997,45(5):217-224
Tumor-associated T cell epitopes are recognized by T cells in the context of determinants specified by class I loci. Since
the rejection of foreign histocompatibility antigens is known to enhance tumor immunity, immunization with a cellular vaccine
that combined the expression of both syngeneic and allogeneic class I determinants could have important immunological advantages
over a vaccine that expressed either syngeneic or allogeneic determinants alone. To investigate this question in a mouse melanoma
model system, we tested the immunotherapeutic properties of B16 melanoma × LM fibroblast hybrid cells in C57BL/6J mice with
melanoma. Like C57BL/6J mice, B16 cells expressed H-2Kb class I determinants and (antibody-defined) melanoma-associated antigens. LM cells, of C3H mouse origin, formed H-2Kk determinants along with B7.1, a co-stimulatory molecule that can activate T cells. The B16 × LM hybrid cells co-expressed
H-2Kb and H-2Kk class I determinants, B7.1 and the melanoma-associated antigens. C57BL/6J mice with melanoma, immunized with the semi-allogeneic
hybrid cells, developed CD8-mediated melanoma immunity and survived significantly (P<0.005) longer than mice with melanoma
immunized with a mixture of the parental cell types. The failure of melanoma immunity to develop in mice injected with the
mixture of parental cells indicated that co-expression of the immunogenic determinants by the same cellular immunogen was
necessary for an optimum immunotherapeutic effect. Augmented immunity to melanoma in mice immunized with the semi-allogeneic
hybrid cells points toward an analogous form of therapy for patients with melanoma.
Received: 19 May 1997 / Accepted: 23 July 1997 相似文献
9.
E. S. Zvezdova T. S. Grinenko E. L. Pobezinskaya L. A. Pobezinsky D. B. Kazansky 《Molecular Biology》2008,42(4):588-597
The specificity of the T-cell receptor (TCR) and its interaction with coreceptors play a crucial role in T-cell passing through developmental checkpoints and, eventually, determine the efficiency of adaptive immunity. The genes for the α and β chains of TCR were cloned from T-cell hybridoma 1D1, which was obtained by fusion of BWZ.36CD8α cells with CD8+ memory cells specific for the H-2Kb MHC class I molecule. Retroviral transduction of the 1D1 TCR genes and the CD4 and CD8 coreceptor genes was used to obtain 4G4 thymoma variants that exposed the CD3/TCR complex together with CD4, CD8, or both of the coreceptors on their surface. Although the main function of CD4 is to stabilize the interaction of TCR with MHC class II molecules, CD4 was found to mediate the activation of transfected cells via TCR specific for the H-2Kb MHC class I molecule. Moreover, CD4 proved to dominate over CD8, since the response of CD4+CD8+ transfectants was suppressed by antibodies against CD4 and the Ab MHC class II molecule but not to CD8. The response of CD4+ transfectants was not due to a cross-reaction of 1D1 TCR with MHC class II molecules, because the transfectants did not respond to splenocytes of H-2b knockout mice, which were defective in the assembly of the MHC class I molecule/β2 microglobulin/peptide complex and did not expose the complex on cell surface. The domination was not due to sequestration of p56lck kinase, since CD4 devoid of the kinase-binding site was functional in 4G4 thymoma cells. The results were used to explain some features of intrathymic cell selection and assumed to provide an experimental basis for developing new methods of anticancer gene therapy. 相似文献
10.
Françoise Albert Michel Buferne Claude Boyer Anne-Marie SchmittVerhulst 《Immunogenetics》1982,16(6):533-549
To study the interactions between T cells and class I MHC products, we developed in vitro a T-cell line reactive to H-2Kb stimulating cells and derived T-cell clones from it. Although the T-cell line could proliferate in the absence of exogeneous T-cell growth factors when stimulated with H-2Kb spleen cells, each of the derived T-cell clones required both H-2Kb stimulating cells and an external source of T-cell growth factor for its propagation. Each of the T-cell clones was also cytolysic for H-2Kb target cells. Such T-cell clones allowed the comparison of the antigenic requirements for proliferation and cytolysis. By using H-2K
b
mutant mice, we found that while the original anti-H-2Kb T-cell line reacted with each of the six mutants tested, the individual T-cell clones could be distinguished in terms of their reactivity pattern. Similar fine specificity patterns were found when H-2K
b
mutant cells were used as stimulating or target cells for any given T-cell clone. Each of the three monoclonal H-2Kb-specific antibodies reacting with different epitopes of the H-2Kb molecule totally inhibited H-2Kb-induced proliferation and lysis by the T-cell clones. Further blocking studies involved use of Fab antibody fragments and definition of their reactivity on cells from the H-2K
b
mutants. We concluded that: (1) blocking with a monoclonal antibody does not prove identity of alloantigens recognized by the T-cells and the antibody; (2) a monoclonal antibody could either block or not block H-2Kb-CTL interactions depending on structural variations of the H-2Kb molecule not affecting the CTL-H-2Kb functional interaction; (3) blocking one type of H-2Kb-T-cell interaction (induction of proliferation) always affects the other type (cytolysis).Abbreviations used in this paper MHC
major histocompatibility complex
- CTL
cytotoxic
- T
lymphocytes
- Th
T helper cells
- PMA
4-phorbol 12-myristate 13-acetate
- Con A
Concanavalin A
- LPS
E. coli lipopolysaccharide
- SCA
Con A stimulated rat spleen-cells supernatant
- SBD
B6 anti-DBA/2 mixed lymphocyte culture supernatant
- TCGF
T-cell growth factors
- IL-2
interleukin 2
- mAb
monoclonal antibody
- FCS
fetal calf serum
- PBS
phosphate buffered saline
- C
complement 相似文献
11.
Mark J. Soloski Ellen S. Vitetta Lorraine Flaherty Jonathan W. Uhr 《Journal of cellular biochemistry》1981,16(2):167-177
The region of the murine 17th chromosome telomeric to H-2D encodes a group of serologically defined cell surface antigens termed Qa-1-5. These antigens are of interest because their expression is restricted to hematopoietic cells. In addition, the molecular weight and subunit structure (ie, association with β-2 microglobulin) of Qa-2 molecules are similar to H-2 and TL antigens. In the present studies, we have prepared isotopically labeled Qa-2 and H-2 molecules from mitogen-stimulated C57BL/6 spleen cells. Comparative peptide mapping of tryptic peptides from Qa-2 and H-2 molecules (Kb, DbKk, Dd) reveal that Qa-2 has a unique primary structure. However, considerable homology is indicated since 30–40% of the Qa-2 peptides cochromatograph with peptides derived from H-2Kb, H-2Db, H-2Kk, and H-2Dd. Studies by other investigators have demonstrated that similar levels of structural homology are observed when H-2K, H-2D, and H-2L tryptic peptides are analyzed. We conclude from these studies that the Qa-2 alloantigen is structurally related to a class of cell surface molecules (ie, H-2) that play critical roles in immune recognition processes. These data further suggest that the genes encoding Qa-2 and H-2 molecules have arisen from a common primordial gene. 相似文献
12.
Aino Laatikainen Henry Karjalainen Henrik Jägerroos Hannu Sarkkinen Rauno Mäntyjärvi 《Cancer immunology, immunotherapy : CII》1990,31(3):164-168
Summary Tumorigenicity in immunocompetent syngeneic mice and H-2 class I antigen expression of BPV1-transformed mouse cell lines had no correlation. H-2 expression was examined using monoclonal anti-(H-2Kb) and anti-(H-2Db) antibodies in immunofluorescence staining for flow cytometry analysis and by determining the sensitivity of the cells to cytolysis by allostimulated spleen cells. Nontumorigenic cell lines were as resistant as tumorigenic cell lines to natural killer activity. The results indicate that in our model defence by natural killer cells is not a decisive factor. The results also show that instead of or in addition to H-2 class I antigens other factors (e. g. the presence or absence of virus-specific antigens) are important in determining the tumorigenicity of BPV1-transformed cell lines. 相似文献
13.
Kevin D. Pavelko Yanice Mendez-Fernandez Michael P. Bell Michael J. Hansen Aaron J. Johnson Chella S. David Moses Rodriguez Larry R. Pease 《PLoS pathogens》2012,8(2)
Structural diversity in the peptide binding sites of the redundant classical MHC antigen presenting molecules is strongly selected in humans and mice. Although the encoded antigen presenting molecules overlap in antigen presenting function, differences in polymorphism at the MHC I A, B and C loci in humans and higher primates indicate these loci are not functionally equivalent. The structural basis of these differences is not known. We hypothesize that classical class I loci differ in their ability to direct effective immunity against intracellular pathogens. Using a picornavirus infection model and chimeric H-2 transgenes, we examined locus specific functional determinants distinguishing the ability of class I sister genes to direct effective anti viral immunity. Whereas, parental FVB and transgenic FVB mice expressing the H-2Kb gene are highly susceptible to persisting Theiler''s virus infection within the CNS and subsequent demyelination, mice expressing the Db transgene clear the virus and are protected from demyelination. Remarkably, animals expressing a chimeric transgene, comprised primarily of Kb but encoding the peptide binding domain of Db, develop a robust anti viral CTL response yet fail to clear virus and develop significant demyelination. Differences in expression of the chimeric Kbα1α2Db gene (low) and Db (high) in the CNS of infected mice mirror expression levels of their endogenous H-2q counterparts in FVB mice. These findings demonstrate that locus specific elements other than those specifying peptide binding and T cell receptor interaction can determine ability to clear virus infection. This finding provides a basis for understanding locus-specific differences in MHC polymorphism, characterized best in human populations. 相似文献
14.
Izumi Nakashima Tomoaki Yoshida Takashi Yokochi Kimiko Ohashi Fumihiko Nagase Ken-ichi Isobe Yoshinori Hasegawa Ko-ichi Ando Reiko Inagi 《Immunogenetics》1986,24(1):32-40
Immunogenicity for T cell-independent B-cell response assessed by splenic plaque-forming cell (PFC) response and cell-surface expression measured by laser flow cytometry of various class I H-2 antigens on mouse red blood cells (RBC) were compared. It was found that the order of magnitude of both immunogenicity and cell-surface expression on RBC is H-2Dd H-2Db > H-2Kd, H-2Kb. Furthermore, H-2d public antigens and H-2Ld antigens were neither immunogenic nor easily demonstrable on RBC. These findings contrasted with poor immunogenicity for PFC response (Nakashima et al. 1982, 1983) and proportionally strong expression of H-2 antigens on lymphoid cells. Immunogenicity and cell-surface expression of H-2Dd antigen on RBC were not shown to be controlled by the action of genes outside H-2D. It was therefore suggested that a number of H-2 antigens, including H-2Kd private, H-2Kb private, and H-2d public specificities are at least functionally defective on RBC. This is possibly due to the structural characteristics of the antigens. Since immunogenicity and cell-surface expression were in parallel, the expression of H-2 antigens on RBC must be dictated by a subset of B cells whose activity was assessed by PFC response. This finding supports the view that the H-2 molecules display a new category of activity which is different from their ability to activate T cells and depends on their expression on RBC. 相似文献
15.
Influenza nucleoprotein (NP) is an important target antigen for influenza A virus cross-reactive cytotoxic T cells (Tc). Here we examine the NP epitope recognized by cloned and polyclonal BALB/c Tc and the genetics of this recognition pattern. We can define NP residues 147–161 as the epitope seen in conjunction with K
d
, the only H-2d class I responder allele for NP restriction. H-2
d
/H-2
b
F1 mice (C57BL × DBA/2) primed by influenza infection lyse only H-2d target cells treated with peptide 147–161 while H-2b targets are recognized only after treatment with NP residues 365–379 (previously found to be recognized by Db restricted Tc cells). Tc cell recognition of NP peptide 147–161 is entirely dictated by expression of K
d
and not by other B10 or OH background genes of congenic mice. Restriction of a unique NP sequence by each responder class I major histocompatibility complex (MHC) allele suggests that antigen and class I MHC interact for Tc recognition. 相似文献
16.
17.
Stavrakoudis A Tsoulos IG Uray K Hudecz F Apostolopoulos V 《Journal of molecular modeling》2011,17(7):1817-1829
Human MUC1 is over-expressed in human adenocarcinomas and has been used as a target for immunotherapy studies. The 9-mer MUC1-9
peptide has been identified as one of the peptides which binds to murine MHC class I H-2Kb. The structure of MUC1-9 in complex with H-2Kb has been modeled and simulated with classical molecular dynamics, based on the x-ray structure of the SEV9 peptide/H-2Kb complex. Two independent trajectories with the solvated complex (10 ns in length) were produced. Approximately 12 hydrogen
bonds were identified during both trajectories to contribute to peptide/MHC complex, as well as 1-2 water mediated hydrogen
bonds. Stability of the complex was also confirmed by buried surface area analysis, although the corresponding values were
about 20% lower than those of the original x-ray structure. Interestingly, a bulged conformation of the peptide’s central
region, partially characterized as a β-turn, was found exposed form the binding groove. In addition, P1 and P9 residues remained bound in the A and F binding pockets,
even though there was a suggestion that P9 was more flexible. The complex lacked numerous water mediated hydrogen bonds that
were present in the reference peptide x-ray structure. Moreover, local displacements of residues Asp4, Thr5 and Pro9 resulted
in loss of some key interactions with the MHC molecule. This might explain the reduced affinity of the MUC1-9 peptide, relatively
to SEV9, for the MHC class I H-2Kb. 相似文献
18.
A new determinant,Qa-m208, detected on T lymphocytes and transfected L cells by a Kb-specific monoclonal antibody 总被引:2,自引:0,他引:2
Margriet Oudshoorn-Snoek Andrew L. Mellor Richard A. Flavell Peter Demand 《Immunogenetics》1984,19(6):461-474
A Kb-specific monoclonal antibody, 6.3.4, defining a new class I specificity, m208, reacts with some K and D region products and with a Qa determinant present on T lymphocytes but not detectable on thymocytes and B lymphocytes. The strain distribution of reactions indicates that this determinant is controlled by the Qa-Tla region, and shows no concordance with the strain distribution pattern of any of the known Qa antigens. The antibody reacts also with L cells expressing a cloned H-2
b
class I gene mapping in the Qa-Tla region. 相似文献
19.
Evidence is presented of the ability of H-2 class I antigens to function as teratocarcinoma transplantation (Gt) antigens. Coisogenic immunization against H-2 class I antigens expressed on transfected L cells is shown to induce resistance to embryonic carcinoma (EC) cell allografts. The Kb, Db, Dd, and, in appropriate recipients, Ld antigens can function as Gt antigens. The protocol presented may be useful for the molecular identification of other genes encoding histocompatibility antigens. 相似文献
20.
John P. Daley Joanne M. Wroblewski Steven G. Kaminsky Ichiro Nakamura 《Immunogenetics》1987,26(1-2):21-30
Hybrid resistance of lethally irradiated (C57BL/6 × DBA/2)F1 and (C57BL/10 × C3H)F1 hybrid mice to the engraftment of parental C57BL/6 or C57BL/10 bone marrow cells is controlled by the H-2-linked Hh-1 locus. This resistance can be specifically blocked or inhibited by the injection of irradiated spleen cells from lethally irradiated, marrow reconstituted donor mice of certain strains. By testing the ability of regenerating spleen cells from various donor strains to block the resistance, we studied the genetic requirements for the expression of putative cell-surface structures recognized in hybrid resistance to H-2b marrow cells. Strains of mice bearing informative intra-H-2 or H-2/
Qa-Tla recombinant haplotypes provided evidence that the Hh-1 locus is located telomeric to the H-2S region complement loci and centromeric to the H-2D region class I locus in the H-2
b
chromosome. Two mutations that affect the class I H-2D
b
gene have no effect on Hh-1
b
gene expression. The H-2D region of the H-2
S
haplotype contains an allele of the Hh-1 locus indistinguishable from that of the H-2D
b
region, as judged by the phenotypes of relevant strains and F1 hybrids. Collectively these data indicate that the Hh-1 locus is distinct from the class I H-2D (L) locus in the H-2
b or H-2
s
genome, and favor the view that the expression or recognition of the relevant determinants is not associated with class I gene products.Abbreviations used in this paper BM(C)
bone marrow (cells)
- CML
cell-mediated lympholysis
- CTL
cytotoxic T lymphocytes
- FBS
fetal bovine serum
- HBSS
Hanks' balanced salt solution
- SC
spleen cells from irradiated, bone marrow-reconstituted mice
Address correspondence to: Dr. I. Najamura, Department of Pathology, School of Medicine, State University of New York at Buffalo, Buffalo, NY 14214, USA 相似文献