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PubMed1963

THYMECTOMY: PROLONGATION OF IMMUNOLOGICAL TOLERANCE IN THE ADULT MOUSE.

The loss of acquired immunological tolerance of mice to bovine gamma globulin depended on the presence of the thymus. Mice were repeatedly injected with bovine gamma-globulin from birth until the age of 5 to 10 weeks and then thymectomized or sham operated. After 130 to 160 days without antigen, an accelerated (immune) disappearance of I(125) bovine gamma-globulin could be uniformly induced in controls while thymectomized mice remained tolerant. Adult thymectomized mice made tolerant by a single injection of bovine gamma-globulin lost tolerance more slowly than sham-operated controls.

Animals↗
PubMed1975

Effect of neonatal thymectomy on experimental subacute sclerosing panencephalitis in adult hamsters.

Syrian golden hamsters were thymectomized in the first 48 h of life, raised, and then inoculated intracerebrally with the HBS strain of hamster-adapted subacute sclerosing panencephalitis virus when over 12 weeks old. Two groups soon become apparent; one group showed progressive neurological susmptoms and the other group remained healthy. The sick hamsters became moribund between days 8 and 17 postinoculation, and they had large amounts of complete virus in their brains, no antibodies to measles virus in their sera, and a demonstrated lack of thymus tissue. Pathological changes in the central nervous system included marked focal necrosis, numerous giant and inclusion-bearing cells, and slight inflammation. The healthy animals, killed at day 22 or 35 postinoculation, contained no central nervous system virus, moderate amounts of measles antibody in their sera, minimal or absent central nervous system pathology, and histologically identifiable remnants of thymus tissue. These studeis indicate that, in the hamster, the immune system is essential in recovering from central nervous system measles infection and that the antibody response to measles probably requires helper T lymphocytes to develop. Im the absence of antibody to measles, the virus did not undergo modification to a cell-associated state, as noted in previous hamster studies and in human subacute aclerosing panencephalitis. This model system may be useful for passive transfer studies to further clarify the effect of the n vivo immune response to acute and persistent central nervous system measles virus infections9

Aging↗
PubMed1982

Effect of neonatal thymectomy on dental caries in rats.

The effect of T-cell depletion on susceptibility to dental caries after infection with Streptococcus mutans was studied. Rats were neonatally thymectomized (Tx) and infected with S. mutans 6715 or locally immunized with the homologous organism before infection. The Tx rats uniformly exhibited a higher level of infection with S. mutans and subsequently showed a greater extent of carious activity. Correlation studies were performed comparing the level of salivary and serum anti-S. mutans antibodies and the relative amount of dental caries. The results demonstrated that salivary immunoglobulin A antibody after immunization and infection, or infection only, showed a significant negative correlation with dental caries. Also, after local immunization, serum immunoglobulin G antibody showed a negative correlation with dental caries in the rats. These findings further support a major protective role for salivary immunoglobulin A in experimental dental caries in rats.

Animals↗
PubMed1992

Dissemination of enteric Mycobacterium avium infections in mice rendered immunodeficient by thymectomy and CD4 depletion or by prior infection with murine AIDS retroviruses.

This study shows that infection of mice with the murine AIDS virus LP-BM5 or Du5H profoundly depressed the capacity of splenic T cells from these animals to respond to the T-cell mitogen phytohemagglutinin or concanavalin A or to alloantigens. Similar effects were also observed if mice were thymectomized and then infused with monoclonal anti-CD4 antibody (TxCD4- mice). When such mice were infected intravenously with Mycobacterium avium, growth of the infection was markedly exacerbated in the TxCD4- mice or in mice given murine AIDS virus 2 months earlier. In view of these data, we then investigated whether such treatments might cause dissemination of M. avium following enteric implantation of bacteria into the mouse cecum; this route was chosen in an attempt to model events in AIDS patients, in which the gut appears to be one of the major portals of M. avium infection. In this model, the entry and hematogenous dissemination of four clinical isolates of M. avium were monitored against time and found to be accelerated and enhanced in T-cell-deficient mice. In view of this finding, these novel approaches for enteric infection that use immunodeficient mice are presented as potential new models for the evaluation of immunotherapy and chemotherapy in a setting that bears some similarity to events believed to occur in AIDS patients.

Animals↗
PubMed2001

Analysis of cytokines in the early development of gastric secondary lymphoid follicles in Helicobacter pylori-infected BALB/c mice with neonatal thymectomy.

Immunological interaction between the host and Helicobacter pylori seems to play a critical role in follicular formation in gastric mucosa. We reported H. pylori-induced follicular gastritis model using neonatally thymectomized mice. In this study, we investigated the involvement of various cytokines in this model. BALB/c mice were thymectomized on the third day after birth (nTx). At 6 weeks old, these mice were orally infected with H. pylori. Histological studies showed that follicular formation occurred from 8 weeks after the infection and that most of the infiltrating lymphocytes were CD4(+) and B cells. Neutrophils increased transiently at 1 week after the infection. Gamma interferon, interleukin-7 (IL-7), and IL-7 receptor were expressed in the stomach of the nTx mice irrespective of the infection. In contrast, expressions of the tumor necrosis factor alpha, IL-4 and lymphotoxin-alpha genes were remarkably upregulated by the infection. Our findings suggest that follicular formation may require cooperative involvement of a Th2-type immune response, tumor necrosis factor alpha and lymphotoxin-alpha in addition to the Th1-type immune response in H. pylori-induced gastritis in nTx mice.

Animals↗