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1.
In the present work, we used the differential redistribution method to study the molecular expression of several H-2 specificities controlled by theD region of theH-2
a
haplotype. We observed that: capping of the private specificity H-2.4 induced capping of the public specificities H-2.3, H-2.35, and H-2.36, and vice versa; capping of any one of these specificities did not induce capping of the public specificity H-2.28, controlled by the same region. By contrast, capping of the H-2.28 specificity induced capping of these specificities; redistribution of H-2K and H-2D private specificities or redistribution of H-2D private specificity and Ia specificities did not induce capping of the H-2.28 specificity. These data indicate that a part of a molecule carrying the H-2.28 specificity is linked to a molecule carrying H-2.4, H-2.3, H-2.35, and H-2.36 specificities and that a part of a polypeptide chain bearing the H-2.28 specificity is independent from that bearing other specificities controlled either by theD region (i.e., H-2.4, H-2.3, H-2.35, and H-2.36) or by theK andI regions. These results further strengthened the hypothesis of the existence of at least two genes controlling theD-region H-2 antigenic specificities. 相似文献
2.
François Lemonnier Catherine Neauport-Sautes François M. Kourilsky Peter Démant 《Immunogenetics》1975,2(1):517-529
Differential redistribution was used to investigate relationships between private specificity H-2.4 and public specificity H-2.28, in the product of aD region allele of theH-2 complex. Monospecific anti-H-2 antisera and fluorochrome conjugated antimouse Ig antibodies were used to induce redistribution of H-2 antigens on the surface of peripheral T lymphocytes fromH-2 a andH-2 d mice. Results showed that redistribution of specificity H-2.4 into patches and caps did not induce concomittant redistribution of specificity H-2.28, which remain diffusely scattered on the cell surface outside the caps of H-2.4. Redistribution of H-2.28 induced redistribution of H-2.4, which was no longer detectable outside the caps of H-2.28. These data indicate that (a) at least some of the H-2.28 sites are expressed on polypeptide chains independent from those carrying H-2.4 and (b) other H-2.28 sites may be linked to molecules carrying H-2.4. Since, onH-2 a cells, both specificities are products of the D region of theH-2 gene complex, our results suggest that there are at least two genes in theD region. 相似文献
3.
The inbred strains GRS/A and LIS/A carry the haplotypeH-2
dx
, which had earlier been shown to have theK
d
,I
f
,S
f
, andG
f
alleles and a previously unknownD region allele,D
dx
. We show here that theD
dx
allele determines a new private specificity, H-2.63, is H-2.28 negative, and determines at least one public specificity of the H-2.1 family. It is thus a second example (afterD
k
) of a H-2.1-positive H-2.28-negativeD region allele. Capping experiments show that the Ddx product comprises two molecules: H-2Ddx bearing the private specificity H-2.63, and H-2Ldx, which is H-2.63-negative but reacts with sera against the H-2.1 family of specificities. SDS gel electrophoresis of detergent-solubilized immunoprecipitated Ddx products shows that the H-2Ldx antigen has a molecular weight of approximately 45,000 daltons and is associated with a smaller polypeptide (mol. wt. 12,000). 相似文献
4.
BALB/c-H-2
db
: A newH-2 mutant in BALB/cKh that identifies a locus associated with theD region 总被引:1,自引:1,他引:0
Ian F. C. McKenzie Gillian M. Morgan Roger W. Melvold Henry I. Kohn 《Immunogenetics》1977,4(1):333-347
A newH-2 mutant, BALB/c-H-2
db
, is described. This mutant originated in BALB/c, is inbred, and is coisogenic with the parental BALB/cKh strain. The mutation is of the loss type since BALB/c-H-
db
rejects BALB/c, but not vice versa. Complementation studies have localized the mutation to theD region of theH-2 complex. A cross between BALB/c-H-2
db
and B10.D2-H-2
da
failed to complement for either BALB/c or B10.D2 skin grafts, indicating that these are two separate mutations at the same locus (Z2). Direct serological analysis and absorption studies revealed that, with one exception, theH-2 andIa specificities of BALB/c and BALB/c-H-2
db
are identical. In particular,H-2.4, the H-2Dd private specificity, is quantitatively and qualitatively identical in the two strains. The exception is that of the specificities detected by antiserum D28b: (k×r)F1 anti-h, which contains anti-H-2.27, 28, and 29. These specificities appear to be absent from theH-2
db
mutant since they are not detected directly or by absorption. Other public specificities are present in normal amounts,e.g., the reaction with antisera to H-2.3, 8, 13, 35, and 36. The reaction with antiserum D28 (f×k)F1 anti-s, which contains antibodies to H-2.28, 36, and 42, is the same in both strains. Antiserum made between the two strains (H-2
db
anti-H-2
d
) reacts like an anti-H-2 serum, in that it reacts with both T and B cells by cytotoxicity, but is not a hemagglutinating antibody. The serum reacts as does the D28b serum in both strain distribution and in cross-absorption studies. We conclude that theH-2
db
mutation occurred at a locus in theD region, resulting in the loss of the H-2.28 public serological specificity and of a histocompatibility antigen. Whether these are one and the same antigen is not yet known. The data, in view of other evidence, imply that the public and private specificities are coded for by separate genes.Abbreviations used in this paper are as follows CML
cell-mediated lysis
- MLR
mixed lymphocyte reaction
- GVHR
graft-versus-host reaction
- RFC
rosette-forming cells
- RAM-Ig
rabbit anti-mouse IgG 相似文献
5.
Thirty B10.W congenic lines were analysed serologically, both by direct cytotoxicity and by absorption, for the presence of H-2L antigens. Three new H-2L antigens, 73, 74, and 75, were discovered. The B10.W lines and the inbred strains can be classified into at least six H-2L phenogroups on the basis of their reactivity withH- 2dm2 anti-H- 2d serum: BALB/c, B10.BUA1, B10.GAA37, B10.BUA16. B10.KPB128, and the negative group. Twenty-oneD-end recom-binants were analysed for the possible separation ofH-2D andH-2L loci. The failure to find such a separation indicates that theH-2D andH-2L loci are tightly linked. Serological analysis also indicated that theH- 2dm1 has lost most of its H-2L antigens but retained at least one specificity which can be detected byH- 2dm2 anti-H- 2d serum. 相似文献
6.
G. M. Morgan H. Dellos I. F. C. McKenzie R. W. Melvold D. W. Bailey 《Immunogenetics》1980,11(1):341-349
Two new C57BL/6H-2 mutants,B6.C-H- 2bm13 and B6.C-H- 2bm14 are described. They arose independently in C57BL/6 as spontaneous mutations of the gain and loss type. Complementation studies map the mutations in both bm13 and bm14 to theH-2D
b
gene. How ever, these two mutant strains are not identical, but occurred as independent mutations at the same locus, as shown by reciprocal graft rejection and by the inability of the (bm13 × bm114)F1 hybrid to accept C57BL/6 grafts. Serological studies by direct testing (cytotoxicity and hemagglutination) and by quantitative absorption demonstrated a decrease in the H-2Db private specificity H-2.2 in both bm13 and bm14 when compared to C57BL/6. This was confirmed by SDS-PAGE analysis using antisera detecting the H-2.2 specificity. Attempts to produce antibodies to either the gained or lost specificities of the two mutant strains failed. 相似文献
7.
Suzanne Ostrand-Rosenberg Craig Hammerberg Michael Edidin Michael I. Sherman 《Immunogenetics》1977,4(1):127-136
Four cell lines derived from four-day-old SWR/J×SJL/J mouse blastocysts have been assayed for their expression of H-2 specificities with pauci- and monospecific H-2 typing sera. Direct microcytotoxicity and indirect absorption studies reveal many deviations from expected expression of particular H-2 specificities based on the cell lines' genotypes and onH-2 typing of adult F1 lymphocytes. No pattern of selective expression of public or private specificities ofD-end orK- end specificities or of inclusion groups was noted. At least one public or private specificity of eachD
q
,K
q
,D
s
, andK
s
region is present, indicating that part of each product is expressed. The partial expression of H-2 specificities is discussed structurally, in terms of how incomplete H-2 molecules may be present on the cell surface, and developmentally, in terms of how the variant H-2 specificities may be involved in cell positioning during ontogenesis. 相似文献
8.
Ian F. C. McKenzie Gillian M. Morgan Roger W. Melvold Henry I. Kohn 《Immunogenetics》1976,3(1):241-251
C57BL/6 (H-2
b
) mice, and four mutants (B6.C-H-2
ba
, B6-H-2
bg1
, B6-H-2
bg2
, B6-H-2
bh
) derived from this strain after separate mutations had occurred at the same locus within theH-2 complex, were analyzed to determine whether the mutations had led to anyH-2 (or Ia) difference which could be detected serologically. The strains were typed directly with antisera specific for H-2K and H-2D public and private specificities and for the Ia specificities; quantitative absorption studies were also performed for the relevant H-2Kb, H-2Dd and Iab specificities. In no case was any quantitative or qualitative difference detected serologically between any of the strains. In addition, by using a variety of techniques to produce and assay for antibody, we failed to produce any antisera between the parental strains and the four mutants. TheH-2 mutations therefore appear to give rise to a type of antigenic specificity which is recognized byT cells and which generateT, but notB cell responses; nor are they recognized by H-2 or Ia alloantisera. The location of the mutating locus within theH-2 complex was shown by the complementation method to be within theK orIA region and not in theIB region, since crosses of the mutant strains with B10.A(4R) or D2.GD failed to complement for a subsequent C57BL/6 skin graft. 相似文献
9.
In comparing the tryptic peptide maps of the H-2L and H-2D glycoprotein antigens isolated from NP-40 lysates of RADA1 (H-2 a ) leukemic cells, no more than 37% of the observed arginine-containing tryptic peptides are found to be homologous. Thus, the primary amino-acid sequences of these two antigens are probably less than 90% homologous. This constitutes the strongest evidence to date that the MHC-linkedH-2L region encodes H-2L antigens separately from theH-2D region, even though H-2L antigens bear D-end-associated antigenic determinants of the H-2.28 family. The anti-H-2.28 alloantiserum (k×r anti h2) used to precipitate H-2L antigens in this investigation was the NIH contract antiserum D28b. As the tryptic peptide maps also surprisingly revealed, D28b precipitates H-2D antigens as well and, thus, anti-H-2.4 immunoadsorbants were employed to isolate H-2L free of H-2D antigens. In light of the dual specificity of D28b, its reactivity with BALB/c-H-2 dm2 mutant cells was re-examined. Even though mutant lymphocytes, which lack H-2L but not H-2D antigens, are not cytotoxically lysed by D28b (as are parental H-2d cells), D28b appears to precipitate H-2D antigens from NP-40 extracts of mutant splenocytes. 相似文献
10.
The molecular relationship between H-2 private and some public specificities was studied in C3H.OH (H-2
02
) mice using surface-antigen re-distribution methods. Besides the Kd- and Dk-region antigens, which can be capped by antisera against the private and public specificities characteristic for a given allele, a previously unknown type of molecule was found in the products of both theK
d
andD
k
regions. These can be capped by the respective anti-private serum but not by antisera against some public specificities. The two Kd-region molecules are provisionally named H-2K1d and H-2K2d. We detected them onH-2
02
(K
d
,I
d
,S
d
,D
k
) and also onH-2
dx
(K
d
,I
f
,S
f
,D
dx
) T lymphocytes. Similarly, the two types of molecules detected on the products of theD
k
region are provisionally named H-2D1k and H-2D2k. The serological characteristics of these molecules are described. When compared with the products of theD
d
region, in which we previously described three different molecules (H-2Dd, H-2Md, and H-2Ld), the mutual relationship between H-2K1d and H-2K2d as well as between H-2D1k and H-2D2k appears to be similar to that between H-2Dd and H-2Md. In the absence of relevant recombinants or informative biochemical data, it is, however, difficult to establish homology between molecules produced by differentK- andD-region alleles. 相似文献
11.
M. Nabholz H. Young T. Meo V. Miggiano A. Rijnbeek D. C. Shreffler 《Immunogenetics》1974,1(1):457-468
B6.C-H-2 ba [H (z1)] is a mutant derived from C57BL/6. The two strains mutually reject their skingrafts and are incompatible in the mixed leucocyte reaction (MLR) and in cell-mediated lympholysis (CML) assays. They are serologically indistinguishable. This report shows that H(z1) carries a new, privateK end CML specificity clearly distinguishable from that of B6 by a third party strain, HTG. Antisera directed against the private H-2K specificity of B6 present on H(z1) cells) can block CML between the two strains in either direction. The new CML specificities of H(z1) cross-react with (public) CML specificities controlled by bothK andD regions of other unrelated haplotypes. The results suggest that H(z1) carries a mutation in theH-2K locus itself or in a closely linked gene, the product of which is also physically associated with the H-2K molecule corresponding to the cis-configuration of the alleles in both loci. These findings indicate that T- and B-cell dictionaries for histocompatibility determinants are different. 相似文献
12.
Evidence for a third,Ir-associated histocompatibility region in theH-2 complex of the mouse 总被引:1,自引:1,他引:0
Skin grafts transplanted from B10.HTT donors onto (A.TL × B10)F1 recipients are rapidly rejected despite the fact that the B10.HTT and A.TL strains should be carrying the sameH-2 chromosomes and that both the donor and the recipient contain the B10 genome. The rejection is accompanied by a production of cytotoxic antibodies against antigens controlled by theIr region of theH-2 complex. These unexpected findings are interpreted as evidence for a third histocompatibility locus in theH-2 complex,H-2I, located in theIr region close toH-2K. The B10.HTT and A.TL strains are postulated to differ at this hypothetical locus, and the difference between the two strains is explained as resulting from a crossing over between theH-2 t1 andH-2 s chromosomes in the early history of the B10.HTT strain. TheH-2 genotypes of the B10.HTT and A.TL strains are assumed to beH-2K s Ir s / k Ss k H-2D d andH-2K s Ir k Ss k H-2D d , respectively. Thus, theH-2 chromosomes of the two strains differ only in a portion of theIr region, including theH-2I locus. The B10.HTT(H-2 tt) and B10.S(7R)(H-2 th) strains differ in a relatively minor histocompatibility locus, possibly residing in theTla region outside of theH-2 complex. 相似文献
13.
MLC were established to test for the generation of specific cytotoxic effector cells in CML. The target cell used to assay for CML in the five combinations tested was of a differentH-2 haplotype from the stimulating cell population. Cytotoxicity was observed against this target only when it shared private alloantigens (antigens that are specific for theH-2D andH-2K region of differentH-2 haplotypes) with the stimulating cell population. Very weak or no Cytotoxicity was found when such alloantigens were not shared, although cross-reactive publicH-2 specificities were. These findings indicate that T cells display a cytotoxic potential against privateH-2 antigens in a primary response in vitro and are not capable of responding to publicH-2 specificities to the same level.BSS
balanced salt solution
- CML
cell-mediated lympholysis
- GPC
guinea pig complement
-
125IUdR
125I-iodo-deoxyuridine
- MLC
mixed lymphocyte culture
- SE
standard error 相似文献
14.
Three newH-2
b
mutant strains, B6.C-H-2
bm9
, B6.C-H-2
bm10
and B6.C-H–2
bm11
, are described. The three mutant strains are of the gain and loss type as they reject skin grafts reciprocally with the parental C57BL/6Kh. The mutations, which arose independently, are all allelic at the same locus as 11 other mutant strains already described. By complementation and other studies the mutated gene has been shown to beH-2K
b
. The strains were typed directly and by absorption with antisera specific for H-2Kb and H-2Db private and public specificities and for Iab specificities. Each strain typed differently with these sera. The strain B6.C-H-2
bm9
was found to be serologically identical with C57BL/6. The strains B6.C-H-2
bm10
and B6.C-H-2
bm11
were found to have alterations in the private H-2Kb specificity, H-2.33, and in the public specificity, H-2.5, but to a different extent. B6.C-H- 2bm10 had a marked decrease in the amount of H-2.33 expressed on the splenic cell surface as compared to C57BL/6 and also has a marked decrease in the expression of H-2.5 on both spleen and red blood cells. In comparison, B6.C-H-2
bm11
has a decrease in the expression of H-2.33 but an increase in the expression of H-2.5 on both splenic and red blood cells. The other H-2b specificities appeared to be unaltered as compared with C57BL/6. 相似文献
15.
Yossef Itzhak 《Molecular neurobiology》1995,11(1-3):217-222
Previous studies proposed the involvement of theN-methyl-D-aspartate (NMDA) type of glutamate receptors in the development of sensitization to the convulsive effect of cocaine (cocaine kindling). The present study was undertaken to determine, first, if cocaine kindling is associated with enhanced sensitivity of the NMDA receptor to the convulsive response ofN-methyl-D,L-aspartate (NMDLA), and second, whether in vivo modulation of nitric oxide synthase (NOS) function regulates the development of cocaine kindling. The following results were observed:
- Cocaine-kindled animals were significantly more susceptible to the convulsive effect of the NMDA receptor agonist NMDLA than saline controls;
- Pretreatment with the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 100 mg/kg; ip) blocked the development of cocaine kindling;
- The protective effect of L-NAME was partially reversed with the coadministration of the NOS substrate,L-arginine (300 mg/kg; ip), but notD-arginine; and
- L-Arginine (300 mg/kg; ip), but notD-arginine, amplified the development of cocaine kindling. Taken together, these findings suggest that supersensitivity of the NMDA receptor and activation of NOS may underlie the development of cocaine kindling.
16.
Serological and capping experiments show that the strain B10.D2 (M504) carrying the mutant haplotypeH-2
dm1
has two molecules in the products of theD region: H-2Ddm1 and H-2Ldm1 which are detectable by anti-H-2.4 and by anti-H-2.28 sera, respectively. Both these molecules differ serologically from the H-2Dd and H-2Ld molecules of the original (nonmutant) strain B10.D2. A third molecule, different from H-2D and H-2L, was detected inH-2
d
,H-2
dm2
but not inH-2
dm1
products. 相似文献
17.
Immune response (Ir) genes mapping in theI region of the mouseH-2 complex appear to regulate specifically the presentation of a number of antigens by macrophages to proliferating T cells. We have investigated the possibility that similarIr genes mapping in theH-2K andH-2D regions specifically regulate the presentation of target antigens to cytotoxic effector T cells. We report that the susceptibility of targets expressing specific non-H-2 H alloantigens to lysis by H-2-compatible, H-antigen-specific cytotoxic effector T cells is controlled by polymorphicH-2K/D genes. This control of susceptibility to lysis is accomplished through what we have defined operationally as antigen-specific regulation of non-H-2 H antigen immunogenicity. High immunogenicity of the H-4.2 alloantigen is determined by a gene mapping in theH-2K region ofH-2
b
. However, high immunogenicity of H-7.1 is determined by a gene mapping in theH-2D region ofH-2
b
. High immunogenicity of the H-3.1 alloantigen is determined by genes mapping in both theH-2K andH-2D regions ofH-2
b
. Therefore, genes mapping in theH-2K andH-2D regions serve a function in presenting antigen to cytotoxic effector T cells. This function is analogous to that played byI-regionIr genes expressed in macrophages which present antigen to proliferating T cells. We present arguments for classification of theseH-2K/D genes as a second system ofIr genes and discuss the implications of twoH-2-linkedIr-gene systems, their possible functions, and their evolution. 相似文献
18.
- The transport of guanine in autospores of light-dark synchronizedChlorella fusca was studied using radioactive guanine in the concentration range of 4 nM to 50 μM.
- The transport system was constitutive, it had high specificity for the permeant, and theQ 10 value was in the range of 1.5 to 2.2. At concentrations lower than 0.2 μM the half saturating constant, S0.5 was 1 μM both for cells kept in dark and cells kept in light. At higher concentrations the S0.5 of darkened cells was about 0.23 μM, while that of illuminated cells was unchanged. Only above 0.2 μM guanine did illumination of the cells or addition of glucose increase the transport rate.
- Guanine which had accumulated did not leak out at temperatures below 45°C or by treatment with 10 μM dinitrophenol, which completely inhibited transport. Furthermore, the accumulated guanine did not exchange with exogenous guanine.
- The guanine accumulated, more than 105-fold over the external concentration, showing that the transport, was active.
- The initial transport rate per cell revealed annual fluctuations.
19.
C. J. M. Melief L. P. de Waal M. Y. van der Meulen P. Iványi R. W. Melvold 《Immunogenetics》1981,12(1):75-88
The fine specificity of cytotoxic T lymphocytes (CTL) directed againstH-2L
d
was analyzed by studying the lytic activity of BALB/cH- 2dm2 (H-2L
d
loss mutant) anti-BALB/c-H-2
d
CTL, generated in secondary mixed lymphocyte culture (MLC) against a panel of target cells of differentH-2 haplotypes. Target cells of allH-2 haplotypes tested, except that of the MLC responder, were lysed by anti-Ld CTL, although to a widely varying extent. The genes coding for antigens detected by anti-L
d
CTL were mapped to distinct regions in theH-2
d
,H- 2dm1,H-2
q
,H-2
k
, andH-2
b
haplotypes. The sequence of lysis intensity against the variousH-2 haplotypes and theH-2 regions involved were as follows:L
d
,D
q
L
q
,D
dm1 Ldm1,K
k
,D
b
L
b
,r, p, f, s, C3H.OH (K
d
D
k
L
k
), strong lysis occurring againstL
d
and weak lysis againstH-2
s
and C3H.OH.By monolayer adsorption and cold target inhibition experiments, it was shown that anti-L
d
CTL contained a CTL subset directed against a private Ld specificity, hitherto undetected by anti-L
d
antibodies. This subset of CTL was separate from the CTL subsets reacting againstH-2
q
and against the mutant haplotypeH- 2dm1. The reactions against the latter two haplotypes were also mediated by separate CTL subsets. It is concluded that the Ld molecule, to a varying extent, shares target antigens for CTL with K- and/or D-end H-2 molecules of all haplotypes tested. These antigens are detected by multiple subsets of anti-L
d
CTL. One CTL subset is directed against a target structure unique forL
d
(Ld private specificity). 相似文献