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V Hauptfeld

Publications and source records attributed to V Hauptfeld.

At least 37 records · Page 2Linked to original sources
PubMed1982

Demonstration of active tolerance in maintenance of established islet of Langerhans allografts.

Streptozotocin-induced diabetes in mice can be reversed by transplantation of islets of Langerhans from histoincompatible mice if the islets are treated with anti-Ia-serum and complement before transplantation. Here we show that anti-Ia-treated islets most likely induce tolerance in the recipient animals. Daily injections of recipient-specific anti-I-J-serum (beginning 80 or more days after transplantation) and small numbers of donor splenocytes caused the prompt rejection of the islets in half of the animals; neither anti-I-J-serum nor donor splenocytes alone were effective. It is likely that rejection of established allografts after this treatment is the result of abolition of the activity of allograft-specific suppressor cells.

Animals↗
PubMed1982

Differences in expression of MHC products between several H-2-restricted CTL clones.

Five cytotoxic T lymphocyte (CTL) clones, all specific for influenza virus A/JAP/57 and all H-2Kd-restricted, were typed for expression of MHC products. All express H-2K and H-2D encoded antigens, but they differ in their expression of I region products. One clone, 14-2, is positive with antisera directed against serologically detectable products apparently related to three different I regions, namely I-A, I-J, and I-E. Two clones, 11-1 and 14-1, lack I-E-associated antigens but express I-A and I-J products, and two other clones, 14-7 and 14-13, lack detectable I region products. These observations show that although discrete CTL clones may be homogeneous in their function, they differ in their expression of I region products.

Animals↗
PubMed1981

Prolongation of murine islet allograft survival by pretreatment of islets with antibody directed to Ia determinants.

Islets of Langerhans treated with donor-specific anti-Ia serum and complement were transplanted across a major histocompatibility barrier into nonimmunosuppressed diabetic mice. The allografts survived in all recipients for at least 200 days after transplantation. Rejection of an established allograft could be induced by intravenous injection of donor splenocytes. This demonstrates that allografts can serve as targets for immune rejection and supports the possible role of Ia-positive passenger lymphoid cells in initiation of immune rejection. The results show that immunosuppression of the recipient is not a prerequisite for successful transplantation.

Animals↗
PubMed1980

Murine pancreatic beta-cells express H-2K and H-2D but not Ia antigens.

Direct microcytotoxicity testing and absorption analyses were employed to determine whether H-2K, H-2D, and Ia antigens are present on murine islet of Langerhans cells. Products of the H-2K and H-2D loci were found on beta-cells from three different mouse strains, but I-region (Ia) antigens were not detected. The absence of Ia gene products from islet cells may be of importance in explaining the survival of islet allografts across major histocompatibility barriers.

Animals↗
PubMed1977

Histocompatibility antigens controlled by the I region of the murine H-2 complex. II. K/D region compatibility is not required for I-region cell-mediated lymphocytotoxicity.

In the cell-mediated lymphocytotoxicity assay, A.TH effector cells sensitized to A.TL lymphocytes lyse not only A.B10.AQR effector cells lyse B10.BR and B10.BYR target cells in addition to B10.AQR cells. These findings indicate that for CML to occur across the IA region barrier, compatibility at K or D regions is not required.

Animals↗
PubMed1977

A new histogenetic method for minor histocompatability antigen typing.

A new method for typing minor H antigens is described. The method is based on the observation that effector T cells, sensitized in vivo to minor H mitigens and then rechallenged in vitro, will lyse labeled target cells in the CML assay, provided that the target, the sensitizing, and the responding cells share the same allele at H-2K or H-2D loci. In this method, two congenic lines differing at a minor H locus are cross-immunized (by skin grafting, injection of lymphoid cells, or, preferably, by a combination of both treatments), rechallenged in vitro, and tested against a panel of strains carrying the same H-2 haplotype as the two lines. Target cells of the panel carrying the same minor H antigens as the strain against which the effector cells were sensitized are lysed; target cells not carrying these antigens are unaffected. The feasibility of the method was demonstrated by testing for H-3 antigens of a panel fo H-2b-bearing strains. The new method is faster and more economical than the classicial F1 method which has been used until recently.

Animals↗
PubMed1976

Histocompatibility antigens controlled by the I region of the murine H-2 complex. I. Mapping of H-2A and H-2C loci.

Skin grafts were reciprocally exchanged in pairs of congenic lines identical in all genes except those located in the central portion of the H-2 complex. Seven such lines were tested: 6R, B10.AQR, A.TL, A.TH, 7R, 9R, and B10.HTT. In all donor-recipient combinations at least some grafts were rejected. In combinations differing at the IA subregion (and other central H-2 regions or subregions), all first-set grafts were rejected within 3 wk after transplantation, and all second-set grafts were rejected within 10 days. In combinations differing at the IC subregion (and other central regions, but not at the IA subregion) between 60 and 100% of first-set grafts were rejected, but some grafts survived for over 100 days. Most of the second-set grafts were rejected within 1 mo after grafting. This behavior of skin grafts indicated the presence of two histocompatibility loci in the I region, a strong one and a weak one. This conclusion was confirmed by genetic mapping which placed the strong locus in the IA subregion and the weak locus in the IC subregion. We designate the former locus H-2A and the latter H-2C. The same strain combinations used for the skin grafting were also used for determination of the capacity of I-region antigens to function as targets in the in vitro cell-mediated lymphocytotoxicity (CML) assay. Spleen cells from mice presensitized in vivo by skin grafting were restimulated in vitro and tested against 51Cr-labeled concanavalin A or lipopolysaccharide blasts. The testing revealed the presence in the I region of two loci coding for CML-target antigens. The two loci comapped with the H-2A and H-2C loci and were most likely identical to them. As in the skin grafting test, in the CML test, the H-2A antigens evoked stronger response than the H-2C antigens. Rejection of skin grafts across the H-2A and H-2C loci was accompanied by the production of Ia antibodies. Direct cytotoxic and absorption tests with Ia antibodies directed against antigens coded for by the IC subregion revealed the presence of IaC antigens on epidermal cells. We suggest that the products of Ia loci might function as transplantation antigens.

Animals↗
PubMed1976

Immunogenetic analysis of H-2 mutations. IV. Mapping of and immune reactions to the H-2fa mutation.

H-2fa is a spontaneous mutation that occurred in an (A.CA X A)F1 female mouse and was later transferred on an A-strain background [congenic line A.CA (M506) or M506]. Skin grafts exchanged between M506 and A.CA strains are rejected within 4 weeks after grafting. Significant reaction is observed when these two strains are used as responders and stimulators in mixed lymphocyte culture or in a splenomegaly graft-versus-host assay. The mutant antigen induces strong cell-mediated lymphocytotoxicity. The mutation maps in the K end of the H-2 complex. The capacity of mutant antigens to induce relatively strong lymphocyte proliferation is explained by hypothesizing that the T-cell receptors reacting with K- or D-region products can more easily recognize subtle than drastic alloantigenic differences.

Animals↗
PubMed1975

Molecular relationship between private and public H-2 antigens as determined by antigen redistribution method.

Molecular relationship of public H-2 antigens 1, 5, 6, 8, 11, 13, 25, and 28 to private antigens controlled by K and D regions was studied using the technique of antibody-induced resistance to complement-mediated cytotoxicity. The results indicate physical association in the cell membrane between H-2 antigens 1 and 23 of H-2-a, 8 and 31 of H-2-d, 11 and 17 of H-2-q, 13 and 30 of H-2-q, 25 and 23 of H-2-k, and 28 and 31 of H-2-g. These results are in agreement with genetic mapping placing the determinants of antigens H-2.8, 11 and 25 in the K region , the determinant of antigen H-2.13 in the D region, and the determinants of antigens H-2.1 and 28 in either the K or the D region. In contrast to genetic mapping placing the determinant for antigen H-2.6 in the D region, we found that in the H-2-b haplotype the antigen is associated with K region antigen H-2.33 and H-2.32, and interpreted this result as evidence for two homologous H-2.5 sites controlled by opposite ends of the H-2 complex. Although the data do not prove that public antigens are carried by the same molecules as private ones, they demonstrate a close physical association in the membrane between the two groups of loci, K and D, coding for the first 33 classical H-2 antigens (with the exception of antigen H-2.7), and thus support the two-locus model. The data also support the duplication model of H-2 by demonstrating two homologous H-2.5 sites associated with K and D molecules.

Animals↗
PubMed1975

Induction of resistance to antibody-mediated cytotoxicity. H-2, Ia, and Ig antigens are independent entities in the membrane of mouse lymphocytes.

Mouse spleen or thymus lymphocytes incubated with monospecific H-2 or Ia alloantisera and then coated with a xenogeneic antimouse Ig serum become specifically resistant to the alloantiserum (and complement) they have been incubated with. This so called "lysostrip method" was used to investigate the molecular interrelationships of antigens in the mouse lymphocyte membrane. The results of this investigation confirm that H-2K and H-2D antigens are carried by two distinct populations of molecules. They provide evidence that the Ia antigens move in the membrane independently of both H2-K and H-2D antigens; and finally they demonstrate absence of any physical linkage between Ig receptors in B cells, on the one hand, and Ia, H-2K, and H-2D molecules on the other hand.

Animals↗
PubMed1975

A method for detection of Ia antigens in the absence of appropriate H-2 recombinants.

A method is described which obviates the use of H-2 recombinant strains for production and detection of Ia antibodies. The antibodies are produced by immunization with spleen cells in a strain combination in which the donor differs from the recipient either in the K end of the H-2 complex or in the whole complex. If the right schedule is used, this immunization produces antibodies against both H-2 and Ia antigens. The H-2 antibodies are absorbed out with erythrocytes or T lymphocytes rendering the antiserum specific for Ia antigens. The presence of Ia Ia antibodies is asserted by determining the tissue distribution of the antigens detected with the absorbed antiserum. Another antiserum is then prepared in the same strain combination by immunization with tissue that does not contain Ia but does contain H-2 antigens (e.g., a sarcoma of the proper genotype). The second antiserum contains only H-2 antibodies and the presence of these antibodies is again asserted by determining the tissue distribution of the corresponding antigens. The molecular distinctiveness of the putative Ia and H-2 antigens is then demonstrated by the newly developed technique of antibody-mediated induction of resistance to cytotoxicity (lysis). If the antigens detected with the two antisera move independently in the cell membrane, and if the antigens detected with the first antiserum do indeed have Ia-like properties, it is concluded that the antiserum detects Ia antigens. This method should prove to be useful for detection of Ia antigens in H-2 haplotypes for which no intra-H-2 recombinants are known, and for detection of Ia-like antigens in other mammalian species, particularly in man.

Absorption↗
PubMed1975

Immunogenetic analysis of H-2 mutations. III. Genetic mapping and involvement in immune reactions of the H-2ka mutation.

Mutation M523 (H-2ka) occurred spontaneously in strain CBA/CaLacSto and was discovered during routine skin graft testing for genetic homogeneity. By linkage and complementation tests, the mutation was previously mapped in the K end of the H-2 complex. We demonstrate that the mutation occurred in the K region, without affecting the I region in the K end of the complex. The mutant antigens cause rejection of skin grafts, stimulate cells in mixed lymphocyte culture, and function as stimulators as well as targets in cell-mediated lymphocytotoxicity. Yet, they are serologically indistinguishable from the antigens of the original strain and do not induce formation of humoral antibodies upon immunization of the CBA strain. Together with the results obtained on testing of other H-2 mutants, the data strongly support the notion that classical H-2 antigens (i.e., products of the H-2K and H-2D loci) can function as lymphocyte-stimulating determinants, and that I-region differences are not required for the induction of strong cell-mediated lymphocytotoxicity.

Animals↗
PubMed1974

Serological distinction of mutants B6.CH(zl) and B6.M505 from strain C57BL-6.

A quantitative serological difference was found between strains Hz1 and M505 carrying mutant H-2 haplotypes ba and bd, respectively, and the original strain B6(H-2(b)). The finding suggests that the mutations occurred in the H-2K(b) gene, and together with data on MLR and CML challenges the current concept of H-2 regions' involvement in immune reactions.

Animals↗