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Biomedical subjects

N L Letvin

Publications and source records attributed to N L Letvin.

At least 253 records · Page 14Linked to original sources
PubMed1984

Common tree shrews and primates share leukocyte membrane antigens.

Monoclonal antibodies reactive with human peripheral blood lymphocyte and myeloid cell surface antigens were utilized to study the phylogeny of the common tree shrew. Blood cells from the common tree shrew, but not the bat or short-tailed shrew, react with certain of these antibodies. These data strengthen the argument that the Tupaiidae are primitive primates rather than insectivores. They also indicate that this approach should be useful for further work in taxonomic systemization.

Animals↗
PubMed1984

Prevention of experimental allergic encephalomyelitis (EAE) in the SJL/J mouse by whole body ultraviolet irradiation.

The cellular requirements for the in vivo induction of experimental allergic encephalomyelitis (EAE) were investigated in the SJL/J mouse. Exposure of mice to whole body ultraviolet (UV) irradiation, a treatment that has been shown in other systems to interfere selectively with antigen-presenting cell function, prevented the development of clinical and pathologic signs of acute EAE. Splenic T cells from UV-treated animals did not adoptively transfer resistance to EAE, making it unlikely that UV irradiation resulted in the generation of a specific suppressor cell population responsible for protection from EAE. UV irradiation was effective in preventing EAE when administered before initial immunization; UV irradiation was ineffective in modifying ongoing EAE or in preventing relapses of EAE induced by reimmunization. In additional experiments, adult thymectomized, lethally x-irradiated mice reconstituted with syngeneic marrow cells depleted of mature T lymphocytes were found to be resistant to the induction of EAE. Susceptibility was restored by the addition of splenic T cells, demonstrating that EAE induction is T cell-dependent in the mouse. The prevention of an experimental autoimmune demyelinating disease by whole body UV irradiation suggests that interference with the function of Ia-bearing accessory cells may represent an approach for immunotherapy in autoimmune disorders.

Animals↗
PubMed1984

Morphologic changes in lymph nodes of macaques with an immunodeficiency syndrome.

Lymph nodes from macaque monkeys with an immunodeficiency syndrome were examined by electron microscopy and both routine histologic and immunoperoxidase staining techniques, using monoclonal antibodies that recognize specific primate lymphocyte subsets. In the early stages of disease, marked follicular hyperplasia and a reduced paracortex comprised predominantly of T8-positive (suppressor/cytotoxic) cells were observed. In monkeys with more advanced disease, lymph nodes showed follicular involution and loss of B cells. Vasculature was seen prominently in the paracortex of these nodes; cellular elements included a mixture of small lymphocytes and larger cells, which by ultrastructural criteria appeared to be lymphoblasts. Lymph nodes in terminal stages of this disease showed a total effacement of architecture with a marked depletion of lymphocytes. These findings are remarkably similar to the lymph node changes seen in humans with acquired immune deficiency syndrome and underline the importance of this disease in macaques as a model for studying acquired immunodeficiency states.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Experimental transmission of macaque AIDS by means of inoculation of macaque lymphoma tissue.

Acquired immuno-deficiency syndrome (AIDS) of macaques, an animal model for human AIDS, was transmitted to previously healthy macaque monkeys by means of inoculation of either tissue or a cell-free filtrate of a macaque lymphoma. The recipients showed evidence of profound lymphocyte dysfunction or died with infections from such opportunistic agents as Candida albicans, Cryptosporidium, and cytomegalovirus.

Acquired Immunodeficiency Syndrome↗
PubMed1983

T lymphocyte surface antigens in primates.

We examined the binding of peripheral blood mononuclear cells from various primate species to a panel of monoclonal antibodies with specificity for human T lymphocytes. A remarkable structural conservation of the erythrocyte rosette receptor on T cells between such phylogenetically distant primates as lemurs and man was found. Furthermore, it was demonstrated that the degree of sharing of other T cell-specific surface determinants between man and other primates reflects the phylogenetic distance between them. Moreover, these studies suggest the potential use of monoclonal antibodies for further structural and functional elucidation of T lymphocyte-specific surface structures.

Animals↗
PubMed1983

Transmission of naturally occurring lymphoma in macaque monkeys.

Spontaneously occurring rhesus monkey lymphomas were transmitted into healthy rhesus monkeys by using tumor cell suspensions. The naturally arising tumors included an immunoblastic sarcoma and an undifferentiated lymphoma. Recipient animals developed undifferentiated lymphomas, poorly differentiated lymphomas, or parenchymal lymphoproliferative abnormalities suggestive of early lesions of lymphoma. Some of these animals developed such opportunistic infections as cytomegalovirus hepatitis and cryptosporidiosis. They also showed evidence of an abnormal circulating peripheral blood mononuclear cell. These findings, all characteristic of the acquired immune deficiency syndrome (AIDS) of macaques, suggest a link between these transmissible lymphomas and AIDS in macaque monkeys.

Animals↗
PubMed1983

Acquired immunodeficiency syndrome in a colony of macaque monkeys.

A naturally occurring immunodeficiency syndrome has been seen in a captive colony of macaque monkeys. This syndrome is seen primarily in the species Macaca cyclopis. Affected animals died with lymphomas (a rare disease in macaques) or such opportunistic infections as Pneumocystis carinii and noma (necrotizing gingivitis). These M. cyclopis exhibited anemia, neutropenia, and a circulating bizarre immature monocyte. In addition, liver function tests suggested hepatitis. Pokeweed mitogen-, concanavalin A-, and xenogeneic cell-stimulated proliferative responses by lymphocytes of animals with the syndrome were dramatically diminished. The T4 (helper, inducer)/T8 (suppressor, cytotoxic) ratio in the peripheral blood mononuclear T-cell populations of M. cyclopis in this colony are decreased when compared with those from either Macaca mulatta in the same colony or normal humans. Epidemiologic evidence implicates a common source agent in this syndrome. The similarity of this syndrome in macaques to human acquired immunodeficiency syndrome suggests that it may provide an important model for studying the human syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Histopathologic changes in macaques with an acquired immunodeficiency syndrome (AIDS).

The authors recently described the clinical course of an Acquired Immunodeficiency Syndrome (AIDS) in a colony of macaque monkeys. In the present study, they have reviewed the histopathology of tissues obtained from a cohort of 16 animals with this clinical syndrome at necropsy. They found evidence in these animals of several opportunistic infections, including cytomegalovirus (CMV), simian virus 40 (SV-40), and noma. Furthermore, a number of other unusual pathologic processes were noted. In 4 animals an array of lymphoproliferative disorders was observed, ranging from multiple nodules of lymphocytes in the kidney, liver, and bone marrow, to frank lymphoma. Evidence of retroperitoneal fibrosis was found in 3 of the animals. Finally, amyloidosis was observed in several animals; in two instances it was present only in the mucosa of the small intestine.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Conservation of myeloid surface antigens on primate granulocytes.

Monoclonal antibodies reactive with myeloid cell surface antigens were used to study evolutionary changes in granulocyte surface antigens from primate species. Certain of these granulocyte membrane antigens are conserved in phylogenetically distant species, indicating the potential functional importance of these structures. The degree of conservation of these antigens reflects the phylogenetic relationship between primate species. Furthermore, species of the same genus show similar patterns of binding to this panel of anti-human myeloid antibodies. This finding of conserved granulocyte surface antigens suggests that non-human primates may provide a model system for exploring uses of monoclonal antibodies in the treatment of human myeloid disorders.

Animals↗
PubMed1982

An adherent cell lyses virus-infected targets: characterization, activation, and fine specificity of the cytotoxic cell.

We have previously reported that mice with defective T lymphocyte function clear a primary reovirus type 1 infection in a normal fashion. The present studies were initiated to determine what cells may play a role in the clearance of this primary infection. We show that macrophages from unprimed mice are capable of lysing reovirus type 1-infected target cells in the absence of specific antibody. Macrophages from nu/nu mice have higher levels of this lytic activity than macrophages from nu/+ and normal mice. In addition, PEC from endotoxin nonresponsive C3H/HeJ mice have virtually no anti-viral lytic activity, while PEC from C3H/FeJ mice have high levels of such activity. Incubation of PEC from C3H/HeJ mice overnight in Con A supernatants restores this lytic activity. PEC are capable of lysing reovirus type 1-infected target cells but not those infected with type 3 reovirus. Using intertypic recombinant viruses, we show this striking target cell specificity to be a property of the sigma 1 protein, the viral hemagglutinin.

Animals↗
PubMed1981

B-lymphocyte responses to trinitrophenyl-conjugated Ficoll: requirement for T lymphocytes and Ia-bearing adherent cells.

These studies were done to characterize the cellular requirements for B-lymphocyte responses to the haptenated polysaccharide trinitrophenyl-conjugated Ficoll. By using an in vitro microculture system, it was demonstrated that hapten-specific anti-trinitrophenyl-conjugated Ficoll plaque-forming cell responses by B lymphocytes require Ia-bearing adherent accessory cells and Thy 1+ Lyt 1+2- nylon wool-nonadherent (T) lymphocytes. Such T cells could be primed in vivo with nonderivatized Ficoll to show carrier-specific helper cell function for derivatized Ficoll responses in vitro. The implications of these findings for our understanding of b-lymphocyte triggering by so-called T-independent antigens are discussed.

Animals↗
PubMed1981

T lymphocyte immunity to reovirus: cellular requirements for generation and role in clearance of primary infections.

The cellular requirements for the development of an immune response to reovirus type 1 and the role of such a response in the clearance of a primary infection with that virus were explored. An Ia-bearing antigen-presenting cell requirement is demonstrated for the in vitro generation of secondary anti-reovirus cytolytic T lymphocytes (CTL). It is then shown that mice whose spleens are depleted of Ia-bearing adherent cells by exposure in vivo to ultraviolet (UV) radiation exhibit depressed priming for reovirus-specific T lymphocyte function-CTL generation, delayed-type hypersensitivity reactivity, and T cell proliferative responsiveness. These UV-irradiated mice clear primary systemic reovirus infections as readily as normal mice. Further, athymic 'nude' mice show no defect in their ability to clear a reovirus infection. The implications of these findings for our understanding of the role of virus-specific T cell function in the clearance of systemic viral infections are discussed.

Animals↗
PubMed1981

Plaque-forming cell responses to trinitrophenyl (TNP)-L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) in microcultures are not under conventional Ir gene control.

The IgM plaque-forming cell response to trinitrophenyl (TNP)-conjugated L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) was studied in an in vitro microculture system. Contrary to expectations, this response was not found to be under conventional H-2 linked Ir gene control. Thus, both classical responder BALB/c (H-2d) and non-responder DBA/1 (H-2q) spleen cells gave equivalent anti-TNP PFC responses to TNP-GAT in these cultures. Experiments were performed to determined if haptenation had changed the GAT carrier so as to remove it from GAT-specific Ir gene control. It could be demonstrated that TNP-GAT elicited in vivo anti-GAT PFC responses showing typical Ir control in the BALB/c and DBA/1 strains; that anti-hapten and anti-carrier PFC responses to DNP-GAT in vivo were similarly controlled; and that the TNP-GAT compound remained a T cell- and Ia+ accessory cell-dependent antigen in vitro. Furthermore, the microculture system allowed GAT-specific T helper cells to be detected in the spleens of DBA/1 mice treated with GAT in vivo under conditions eliciting a predominant suppressor T cell response under usual conditions of assay. These findings contrast with the Ir gene regulation of TNP-(T,G)-A--L responses seen under identical culture conditions. The implications of these results for our understanding of the site of Ir gene action and the target of suppression in the GAT model are discussed.

Animals↗
PubMed1980

Immunologic effects of whole-body ultraviolet irradiation: selective defect in splenic adherent cell function in vitro.

Splenocytes from mice receiving whole-body UV irradiation do not make a normal primary in vitro plaque-forming cell (PFC) response to the soluble T-dependent antigen trinitrophenylated poly(L-glutamic acid60L-alanine30L-tyrosine10). This impaired immune response results from a selective loss of antigen-presenting cell function in the splenic adherent cell (SAC) population of the UV-treated mice. SACs from UV-irradiated mice are unable to reconstitute a PFC response when added to normal splenocytes passed through Sephadex G-10 (which depletes adherent cells), whereas normal SACs, when added to Sephadex G-10-passed splenocytes from UV-treated mice, do restore a PFC response. The effect of in vivo UV irradiation on the SAC population is indistinguishable functionally from the effect of in vitro UV irradiation of SACs from normal mice. Possible explanations for this selective effect of external UV irradiation on SAC function are discussed.

Animals↗