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[Immunogenetic analysis of Cryptomeria pollinosis. Evidence for the HLA-linked immune suppression gene to Cryptomeria japonica pollen antigen].

The IgE response to Cryptomeria japonica pollen antigen (CPAg) in vivo was measured by radioimmunoassay, using plasma from 525 members of 98 families. 1) The 525 were classified into non plus low (non/low) responder group and high responder group. 2) Segregation analysis revealed that the non/low responsiveness to CPAg was formally a single dominant trait. 3) The frequency of this gene mediated for non/low responsiveness to CPAg was calculated to be 0.44-0.60. 4) Linkage analysis revealed that the gene controlling non/low responsiveness to CPAg is linked to human leukocyte antigen (HLA) with a maximum lod score, 3.40 at theta = 0.18. 5) Non/low responders' macrophage could present CPAg to B.T cell of high responders in an HLA-DR-shared combination. A foregoing study demonstrated that HLA-DR molecule function as a product of Ir-gene for CPAg and that the non/low response to CPAg was mediated by CPAg-specific suppressor T cells. Taken together, these observations clearly demonstrated that the non/low responsiveness to CPAg is not due to the defect of Ir-gene, but rather is mediated by the HLA-linked immune suppression gene for CPAg (Is-CPAg), through CPAg-specific suppressor T cells. This is the second report for HLA-linked Is-gene in humans.

Female↗

Familial polyarteritis nodosa: a serologic and immunogenetic analysis.

Familial polyarteritis nodosa (PAN) is a rarely described entity. We describe a family with 2 members with PAN after a common hepatitis B infection. Many other autoimmune diseases and autoantibodies were found in other family members not corresponding to HLA phenotypes, suggesting other non-HLA-linked genetic influences may be operative in predisposition to PAN.

Adult↗

Immunogenetics of insulin-dependent diabetes mellitus in humans.

Diabetes mellitus is the second most prevalent chronic disease in children in the U.S. It is associated with severe manifestations which include blindness and circulation deficiencies as well as markedly increased risk of death. The etiology of diabetes mellitus remains a mystery although both genetic and environmental factors have been implicated. The geneticist is confronted with a number of obstacles in his attempts to unravel this problem, including differences in the definition of affected individuals. This matter was certainly clarified by the separation of noninsulin-dependent diabetes (NIDDM) and insulin-dependent diabetes mellitus (IDDM) into two separate disease entities. Twin studies, however, show that IDDM cannot be entirely due to genetic causes as concordance is no more than about 50%. Although the disease is then clearly not inherited per se, the "susceptibility" to diabetes seems almost surely inherited and, provided this susceptibility, the disease can be brought on by environmental factors. Until the underlying mechanism causing IDDM is completely ascertained, we have to rely on genetic markers to approach the study of the inheritance thereof. Since, in the early 1970s, research by Nerup's and Cudworth's groups revealed associations between the HLA-B locus and IDDM, the HLA markers are considered the classical genetic markers for IDDM susceptibility. In this paper, we review the nature of the genetic susceptibility to IDDM and the possible environmental factors which can bring on the disease.

Animals↗

[Immunogenetic study of porcine IgG].

Three allotypes of IgG were identified in pig. Based on data obtained on electrophoretic mobility as well as on results of the International Comparative Test ISABR for pig blood group, polymorphic proteins and enzymes (1987-1988), the allotypes are specified as markers of two different IgG subclasses and are referred to as IgG1a, IgG2b and IgG2c. The former of these is established as corresponding to the already known IGH3 C1, and the other two had not been earlier described. In herds of pigs being bred in the Georgian SSR, the IgG1a allotype frequencies in Kakhetinskaya, Large White, Landrase and Lithuanian white were 0.84, 0.93, 0.91 and 0.94, respectively, whereas for the IgG2b allotype it ran 0.89, 0.73, 0.79, and 0.69 in the order mentioned. The IgG2c allotype was not registered in samples under examination.

Alleles↗

[Immunogenetics of Horton's disease and of rhizomelic pseudo-polyarthritis].

The etiopathogenesis of temporal arteritis and rhizomelic pseudo-polyarthritis still remains undefined. A genetic predisposition would seem probable in view of epidemiological data (higher frequency in white caucasian races and in certain countries), the existence of rare familial forms (25 families reported), and the significant increase in incidence in unconnected cases with HLA DR4 antigen (6 studies). Environment may intervene as a precipitating factor in the condition and the role of an infectious agent, to account for the seasonal incidence of this disorder and the rare existence of cases in non consanguineous couples, has been suggested but remains unproven. Disordered immune function probably plays an essential role in the creation of the vascular histological lesions characteristic of the condition. The disordered function involves cellular immunity (fall in OK T8. in blood) and especially humoral immunity with the very frequent presence of circulating immune complexes in the serum and deposition of immunoglobulins and complement at arterial wall level.

Antibody Formation↗

Spontaneously metastasizing rat sarcomas LW13K2 and RPS: assessment by the immunogenetic test of malignancy, in vitro behaviour and karyology.

Populations of LW13K2 sarcoma derivatives were compared for their malignancy, patterns of cell behaviour in vitro (dynamic morphology and migration) and karyological pattern. The following tumour cell populations were used: the original LW13K2 sarcoma from inbred LEW/CUB rats, RPS sarcoma derived from it by neoplastic progression, four cell populations isolated in vitro from metastases of a syngeneic LEW-CUB strain rat with RPS tumour and four neoplastic cell populations isolated from spontaneous metastases shed by RPS sarcoma in allogeneic rats, differing from LEW/CUB in weak alloantigenic loci. Although RPS tumour did not grow progressively in MHC-different recipients (while the original LW13K2 tumour did), it grew progressively and metastasized in all groups of non-MHC allogeneic recipients. Parallel with the metastatic potential patterns of in vitro behaviour, such as an increased incidence of the quasi-stellate morphotype at slightly acid culture conditions endowed with enhanced changeability of the cell shape and migrational activity, were found. Cytogenetic analysis demonstrated rather stable chromosomal patterns over the cascade of neoplastic progression from LW13K2 sarcoma over RPS sarcoma to freshly isolated metastases. This indicated that the apparent neoplastic progression observed in the cell populations derived from LW13K2 sarcoma is with high probability not due to the selection at the chromosomal level.

Animals↗

[A new immunogenetic marker of rheumatism].

Use of monoclonal D8/17 antiserum was studied for identification of B-cell antigen in 44 rheumatic fever patients. The control group comprised healthy subjects (30) and patients suffering from rheumatoid arthritis (30), ischemic heart disease (IO); chronic tonsillitis (12) and different neoplasma of the brain (10). The preliminary genetic analysis of these patients has shown that monoclonal antiserum D8/17 can identify B-cell marker in 88-100 per cent of rheumatic fever cases.

Adolescent↗