It has been postulated and experimentally supported that some idiopathic recurrent spontaneous abortions are caused by recessive lethal genes, probably linked to the major histocompatibility complex. The biggest problem in a trait analysis of some hereditary phenotypic characteristic or disease is genetical heterogeneity. The other problem is a possibility that the predisposition for disease is autosomal dominant characteristic, although disease is caused by recessive genes. In order to investigate genetics of idiopathic recurrent spontaneous abortions and defective reproductive fitness as a separated and unique clinical and immunologycal entity, 122 couples with two or less (44 couples), three or more (19) spontaneous abortions, blighted ovum or missed abortion (14), malformed child with or without spontaneous abortion (32) and sterility (13), were cytogenetically and genetically analysed. All gynaecological and hormonal causes are ruled out previously. Overall frequency of major chromosomal aberration is 13.1% (16/122) and 18% (22/122) for the chromosomal variants. Although, it is not still clear if the chromosomal variants or duplication of heterochromatin can interfere with reproductive fitness, those couples are also excluded because the content of heterochromatin of couples with malformed child with or without spontaneous abortion is significantly higher than in the control group (9 couples with one or more children and with no history of sp.ab.). The family pedigree of couples with familial spontaneous abortion shows vertical, no sex-related expression through several generation and no consanguinity, what leads us to conclusion that idiopathic recurrent spontaneous abortion or its predisposition has autosomal dominant trait. The next step will be to see if those genes are HLA-related or not.
To establish the role of T-lymphocyte subpopulations in the processes of liver regeneration following partial hepatectomy (pHx)and vice versa, the effect of factors produced in regenerating liver on lymphatic tissue, a series of studies has been conducted.Specifically, in this work we have analyzed (a) the consequences of in vivo depletion of CD4+ and CD8+ lymphocytes on hepatic DNA, RNA, and proteins ; and (b) the consequences of pHx on phenotypic profile of cells in spleen of mice depleted of CD4+ and CD8+ lymphocytes. The data revealed that depletion of CD8 and depletion of both CD4-and CD8-positive T lymphocytes significantly augment the content of hepatic proteins and RNA in regenerating liver. The latter treatment translocated also the peak of protein synthesis from second to firs post-Hx day. On the other hand, pHx stimulated the recovery of CD4+ cells in CD4-depleted mice and augmented the proportion of CD8+ cells in both CD8- and CD4+CD8-depleted mice. The data point to the existence of hepatoregulatory lymphatic cells or cytokines and to the hepatic origin of substances that lead to the induction of lymphocytes with morphogenetic properties.
Development of the lymphoid cell compartment in bronchus-associated lymphoid tissue (BALT) of specific pathogen free chickens was examined. Specifically, B lymphocytes, T cell subsets (CD4 and CD8), and IgA-, IgG-, and IgM-producing plasma cells were labeled using immunocytochemical methods. Immunoglobulin-producing cells (IgPC) were quantitated, and comparisons of IgPC numbers were made among chickens of different ages, among immunoglobulin isotypes, and between lymphoid (BALT) and nonlymphoid (non-BALT) areas in the primary bronchus. At hatching, BALT was devoid of IgPC, but by 2 weeks of age cells producing IgA, IgG, and IgM were present. Initially, there were approximately equal numbers of IgA-, IgG-, and IgM-PC; after 2 weeks of age, however, IgG- and IgM-PC outnumbered IgA-PC. At all ages, IgPC were more numerous in non-BALT regions of the primary bronchus than in BALT regions. Small numbers of T and B lymphocytes were present in BALT from 1-day old chickens, but substantial populations of these cells were not seen until 1-2 weeks of age. T helper (CD4+) cells were found near B cell regions in BALT lymphoid nodules, while T cytotoxic/suppressor (CD8+) cells were more evenly distributed throughout the nodules and in the epithelium. B lymphocytes predominated in germinal centers and also overlapped CD4+ populations adjacent to germinal centers. Lymphocyte cell types needed to initiate and regulate immune responses are present in chicken BALT and may be involved in protecting poultry from respiratory pathogens.
Previous work in our laboratory has shown that fetal protection from maternal transmission of the murine lactate dehydrogenase-elevating virus (LDV) infection is mediated by adoptive transfer of maternal anti-viral immunity. In the present report, we have characterized reconstitution of immunity in immunodeficient SCID mice following transplantation with BALB/c spleen cells, and studied the fate and distribution of maternally-derived antibodies after passage to neonatal SCID mice by nursing. Immune-reconstituted SCID mice maintained stable immunity for up to 7 months post-transplantation, during which time they produced nonneutralizing IgG anti-LDV antibodies and protected their offspring from maternally-derived LDV infection. Using IgG isotype and allotype assays, it was found that maternal IgG antibodies transferred from breast milk to nursing neonatal mice and appeared in their circulation. Weaning of SCID mice from immunocompetent mothers permitted the determination of blood immunoglobulin isotype half-lives (3.6-10.6 days) in the absence of endogenous antibody production. LDV infection was transferred to nursing mice by nonimmune LDV-infected mothers, but protection from nursing-acquired LDV infection was associated with maternal viral immunity, breast milk transfer of IgG anti-LDV to nursing mice, and reduced breast milk virus titers. These findings show a nursing pathway for LDV infection, and demonstrate the potential of immune protection from this infection pathway.
