Complementation of H-2-linked genes controlling immune responsiveness

Dorf, Martin E.

doi:10.1007/bf01892406

Cited by 38 publications

(19 citation statements)

References 91 publications

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“…For many immunogens the immune responsiveness found in Fl mice but in neither parental inbred mouse strain is the consequence of gene complementation of the class II histocompatibility molecules (1,2). Though abundant evidence exists that analogous dimeric af3 molecules are present in man (3)(4)(5), examples ofgene complementation demonstrating an in vivo human immune response are lacking.…”

Section: Introductionmentioning

confidence: 99%

HLA-DQ gene complementation and other histocompatibility relationships in man with the anti-Ro/SSA autoantibody response of systemic lupus erythematosus.

Fujisaku¹,

Frank²,

Neas³

et al. 1990

J. Clin. Invest.

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A strong gene interaction between HLA-DQ1 and DQ2 alleles has been associated with anti-Ro/SSA autoantibodies ( HLA-DQ1/DQ2 heterozygotes is most closely related to antiRo/SSA autoantibodies, thereby supporting a gene complementation mechanism. Beyond this effect, an RFLP associated with HLA-DQ2 and/or DR7 is also related to Ro/SSA precipitins. Multiple molecular histocompatibility mechanisms are implicated, therefore, in the production of anti-Ro/SSA autoantibodies in autoimmune disease. For anti-Ro/SSA autoantibodies in SLE, and perhaps more generally, these data show that the histocompatibility antigens are among the elements that confer autoimmune response specificity and restrict the production of particular autoantibodies among patients with systemic lupus erythematosus. (J. Clin. Invest. 1990. 86:606-611.)

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Section: Introductionmentioning

confidence: 99%

HLA-DQ gene complementation and other histocompatibility relationships in man with the anti-Ro/SSA autoantibody response of systemic lupus erythematosus.

Fujisaku¹,

Frank²,

Neas³

et al. 1990

J. Clin. Invest.

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“…There are several reports of F1 hybrids produced from matings of two low-responder parental strains giving responses higher than the response of either parental strain (37,38). Our data show that hybrid mice (lAk X IAbml2) respond very well to beef insulin (Table 3).…”

Section: Mapping Of Genes Controlling Proliferative Response Tomentioning

confidence: 99%

Selective loss of antigen-specific Ir gene function in IA mutant B6.C-H-2bm12 is an antigen presenting cell defect.

Lin¹,

Rosenthal²,

Passmore³

et al. 1981

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

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Immune responses to several soluble antigens were compared between B6.C-H-2bmlf mutant and wild-type B6 mice by using a lymph node T-cell proliferation assay. B6.C-H2blf mice failed to respond to beefinsulin whereas other lA genecontrolled responses, such as response to poly(L-Tyr, L-Glu)--poly(DL-Ala, L-Lys) and collagen, were indistinguishable between mutant and wild-type mice. The responses to multideterminant antigens such as ovalbumin and purified protein derivative of tuberculin were also found to be comparable in B6.C-H-2bmla and B6 mice, thus indicating that this mutation resulted in a selective loss of the ability to respond to a certain antigen(s)-e.g., beef insulin. Populations depleted of adherent cells have been used to examine the mechanism by which Ia molecules mediate Ir gene control of antigen recognition. We show that the nonresponsiveness to beef insulin in the mutant mouse is the result of defective antigen presentation. In addition, we find that F1 hybrids between two nonresponders-B6.C-H12bfl2 and B1O.A or B10.AKM (IAk)

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“…The ability of NP-GL to prime for an NP-specific response was then examined. GL is unable to induce an antibody response in all strains of mice thus far examined (5,6). Similarly, NP-GL was unable to prime for an NP-specific response in the four strains examined.…”

Section: Resultsmentioning

confidence: 99%

“…As mentioned previously, mouse strains which respond to GL have not been identified (5,6). The data in Table II demonstrate that the NP-specific response may be easily and efficiently elicited by NP-GL in NP-BGG primed mice.…”

Section: Resultsmentioning

confidence: 99%

Ir gene controlled carrier effects in the induction and elicitation of hapten-specific delayed-type hypersensitivity responses.

Weinberger¹,

Benacerraf²,

Dorf³

1979

The Journal of Experimental Medicine

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We have recently demonstrated that genes in the VH linkage group control the fine specificity of the delayed-type hypersensitivity (DTH) response to nitrophenyl acetyl (NP) (1). It was shown that transfer of reactivity to NP was both T-cell dependent and required I-A homology between the donor and recipient animals (1). The studies described below were undertaken to further clarify the specificity of the responding T cell, as well as the specificity of other cells which could be involved in the DTH pathway.In our earlier studies, cyclophosphamide-pretreated mice were primed with NPbovine gamma globulin (NP-BGG), and NP-specific DTH responses were elicited by challenge with NP on a heterologous carrier, NP-bovine serum albumin (NP-BSA) (1). Because of considerable accumulated evidence from this laboratory of carrier effects in DTH reactivity (2-3), 1 the role of the carrier in the various phases of the NP-specific DTH response was explored. To analyze the carrier requirements in this response more definitively, we chose to use carriers, the immune response to which are under H-linked Ir gene control. The use of such carriers was motivated by the fact that for an Ir-restricted antigen, such as poly-(L-gluS6-L-lys~-L-phe 9) (GL~), strains of mice of the appropriate H-2 haplotype do not manifest detectable immune responses or carrier specific helper function (4, 5). Thus, by examining the effect of this antigen on the various phases of the hapten-specific DTH response in responder and nonresponder strains of mice, we were able to gain insight into the role of the carrier moiety in the induction and elicitation of NP-specifie DTH responses. Materials and MethodsAnimals. All mice were purchased from The Jackson Laboratory, Bar Harbor, Maine, or were bred in the animal facilities of Harvard Medical School. Mice were used at 2-12 mo of age, and were maintained on laboratory chow and acidified, chlorinated water ad libitum.Antigens. The linear terpolymer GL~, lot GLP2, average mol wt 45,000, was prepared by Miles-Yeda, Ltd., Rehovot, Israel. The random linear copolymer, poly-(L-glu6°-L-lys4°), GL, lot 33, was purchased from Pilot Chemicals, Boston, Mass. BSA and BGG were purchased from Sigma Chemical Co., St. Louis, Mo. The preparation of NP-conjugated proteins has been previously described (1). The molar conjugation ratio of haptenic group used in this

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Complementation of H-2-linked genes controlling immune responsiveness

Cited by 38 publications

References 91 publications

HLA-DQ gene complementation and other histocompatibility relationships in man with the anti-Ro/SSA autoantibody response of systemic lupus erythematosus.

HLA-DQ gene complementation and other histocompatibility relationships in man with the anti-Ro/SSA autoantibody response of systemic lupus erythematosus.

Selective loss of antigen-specific Ir gene function in IA mutant B6.C-H-2bm12 is an antigen presenting cell defect.

Ir gene controlled carrier effects in the induction and elicitation of hapten-specific delayed-type hypersensitivity responses.

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