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PubMed1981

Immunogenetics of childhood celiac disease: the association with HDA DR3 and DR7 in unrelated patients with multiply affected families.

The association between childhood celiac disease and the histocompatibility complex was studied in five multiply affected families and 20 unrelated patients. The diagnosis of celiac disease (CD) was established by three consecutive jejunal biopsies: 1) at the initiation of the diagnosis; 2) following a gluten-free diet; and 3) after gluten provocation. The results of this study indicate that a significant association exists between celiac disease, DR3 (P less than 0.001) and DR7 (P less than 0.001). The relative risks for these antigens were 8.56 and 5.05, respectively. Segregation analysis in the families suggested that the susceptibility genes associated with the histocompatibility antigens are not inherited in either a dominant or a recessive pattern. While an intermediate type fits better into the genetic framework of CD, more than one susceptibility and protecting gene may be involved in the pathogenesis of this disease.

Adult↗
PubMed1982

Immunogenetics of BCG-induced anergy in mice: control by genes linked to the Igh complex.

The genetics of BCG-induced anergy was studied in mice by evaluating delayed hypersensitivity to sheep erythrocytes. Data obtained using congenic mice and by linkage analysis suggested that genes linked to the H-2 complex do not influence the development of anergy. However, studies in allotype-congenic partners (BALB/c; BALB.Igb) indicated that anergy was influenced by genes linked to the immunoglobulin heavy chain complex (Igh). Breeding studies indicated that the gene influencing anergy is recessive. These studies were extended by using BXD recombinant inbred mice, and verified that anergy is controlled by genes linked to the Igh complex. Because several markers and a tentative map has been constructed for the Igh complex on chromosome 12 in BXD mice, we suggest that the gene that controls BCG-induced anergy is located on the centrometric side of Igh-C approximately 18 to 28 recombination units.

Animals↗
PubMed1982

Immunogenetic analysis of patients with post-schistosomal liver cirrhosis in man.

Immune responsiveness of 121 patients with post-schistosomal liver cirrhosis to schistosomal antigens was investigated. Out of 78 patients, only five (6.4%) showed low responsiveness to schistosomal adult worm antigen whereas 73 (93.6%) were high responders. Out of 57 healthy individuals with previous schistosomal infection, low responders were found in 17.5%. The frequency of low responders to schistosomal adult worm antigen was significantly decreased in the patients with post-schistosomal liver cirrhosis (P less than 0.05). Out of 121 patients, a significant increase in frequency of HLA-Bw44-DEn haplotype was observed (corrected P less than 0.02). On the other hand, HLA-Bw52-Dw12 haplotype which was reported to be in strong linkage disequilibrium with an immune suppression gene for schistosomal adult worm antigen was significantly decreased (corrected P less than 0.005). These observations suggested that an HLA-linked immune suppression gene controlled susceptibility or resistance to post-schistosomal liver cirrhosis through regulation of immune responsiveness of the hosts to schistosomal antigen in man.

Adult↗
PubMed1981

Immunogenetic studies on the resistance of mice to highly metastatic DBA/2 tumor cell variants. II. Influence of minor histocompatibility antigens on tumor resistance, gamma-interferon induction and cytotoxic response.

B10.D2 mice (H-2d) were found to be able to reject more than 10(6) cells of the DBA/2 (H-2d) tumor ESb, while DBA/2 mice could not reject even small (less than 10(1) cells) tumor cell inocula and died within a few weeks from the developing internal metastases. Chimaeric mice and F1 hybrids between DBA/2 and B10.D2 were susceptible to the tumor and its metastases, suggesting that tumor resistance was dependent on the ability of the host to recognize DBA/2 minor alloantigens. About two thirds of the (DBA/2 X B10.D2) F2 generation mice were ESb tumor-resistant. Also, the majority of C57B1/6 X DBA/2 recombinant inbred strains (BXD RI lines) of H-2d type were found to be able to reject ESb tumor cells. There was no apparent linkage of tumor resistance to coat color genes. Mls locus, or immunoglobulin heavy chain genes. It is suggested that tumor resistance in these mice was dependent on the recognition of several DBA/2 minor histocompatibility antigens such as H-1 and H-4. The most resistant of the BXD RI strains, BXD-6, was shown to react to minor DBA/2 antigens by the production in vitro of interferon and of cytotoxic cells. These cellular immune reactions were not observed in one of the less resistant strains, BXD-28, suggesting a close relationship between tumor rejection and the capability to produce interferon and cytotoxic lymphocytes.

Animals↗