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J Holoshitz

Publications and source records attributed to J Holoshitz.

29 records · Page 2Linked to original sources
PubMed1985

Role of the thymus in induction and transfer of vaccination against adjuvant arthritis with a T lymphocyte line in rats.

Adjuvant arthritis is an experimental disease of rats induced by immunization to antigens of Mycobacterium tuberculosis. Our observation that arthritis could be induced in irradiated rats by the A2 line of T lymphocytes in the absence of mycobacterial antigens suggested that adjuvant arthritis is an autoimmune disease. Moreover, the A2 line could be used to vaccinate unirradiated rats against the subsequent induction of adjuvant arthritis by active immunization to Mycobacteria. In the present study we found that thymus cells obtained from A2 vaccinated rats could transfer resistance to adjuvant arthritis to naive rats. This indicates that the mechanism of resistance induced by A2 vaccination is probably immunological and involves thymus-derived lymphocytes.

Animals↗
PubMed1984

T lymphocyte lines induce autoimmune encephalomyelitis, delayed hypersensitivity and bystander encephalitis or arthritis.

Lines of rat T lymphocytes responsive to the basic protein of myelin (BP) or to the purified protein derivative of Mycobacterium tuberculosis (PPD) were inoculated i.v. into recipient rats. As reported previously, the anti-BP line cells, but not the anti-PPD line cells spontaneously accumulated in the central nervous system and caused encephalomyelitis. However, the anti-PPD line cells could be induced to enter the brain and cause bystander encephalitis by intracerebral inoculation of PPD. Anti-PPD or anti-BP line cells could mediate delayed-type hypersensitivity skin reactions or bystander arthritis elicited by specific antigen. The lines did not cause specific cytolysis in vitro. Susceptibility to delayed-type hypersensitivity or bystander disease was long lasting in rats inoculated with anti-PPD line cells, while rats inoculated with anti-BP line cells were susceptible for only a few days. Thus, lines of T lymphocytes can mediate a variety of pathological reactions directed by the presence of specific antigen, self or foreign.

Animals↗
PubMed1984

Arthritis induced in rats by cloned T lymphocytes responsive to mycobacteria but not to collagen type II.

We have been studying the pathogenesis of adjuvant arthritis in rats using a long-term cell line of T lymphocytes, the A2 line, which can induce polyarthritis and can also be used to vaccinate rats against adjuvant arthritis. Although line A2 was selected for its proliferative response to mycobacteria, it also responded to collagen type II. To elucidate its role of responsiveness to collagen type II and the relationship between arthritogenicity and vaccination, we cloned A2 and selected a subline A2b. We now report that subline A2b, which bore a marker of helper/delayed hypersensitivity T lymphocytes, was strongly arthritogenic, but could not vaccinate against arthritis. Moreover, A2b showed no response to collagen type II. Therefore, reactivity to collagen type II is not a requisite for arthritogenicity, and mediation of arthritis and vaccination can be distinct properties of different populations of T lymphocytes.

Animals↗
PubMed1983

Lines of T lymphocytes induce or vaccinate against autoimmune arthritis.

The pathophysiology of autoimmune arthritis was studied by selecting and isolating lines of effector T lymphocytes from rats administered an arthritogenic dose of Mycobacterium tuberculosis in complete Freund's adjuvant to induce adjuvant arthritis. Irradiated rats were intravenously inoculated with a cell line characterized by proliferative reactivity to Mycobacterium tuberculosis and, to a lesser degree, to rat collagen type II. This produced arthritis in all the irradiated rats. Nonirradiated recipients failed to develop arthritis. However, such rats, and those recovering from cell-mediated arthritis, were resistant to subsequent attempts to induce adjuvant arthritis. Lines of T lymphocytes selected for responsiveness to other antigens had no effect. Therefore, a line of T lymphocytes responsive to bacteria or to collagen type II could either induce autoimmune arthritis or serve as an agent of vaccination against it.

Animals↗
PubMed1983

T lymphocyte lines producing or vaccinating against autoimmune encephalomyelitis (EAE). Functional activation induces peanut agglutinin receptors and accumulation in the brain and thymus of line cells.

We studied lines of rat T cells, specifically reactive against myelin basic protein (BP), that were functional in mediating autoimmune encephalomyelitis or in vaccinating rats against induction of active EAE. Herein we report that these functions depended on activation of the cells by incubation with BP or with a T cell mitogen prior to inoculation into recipient rats. Activation was accompanied by the exposure of membrane-binding sites specific for the lectin peanut agglutinin. Accumulation of activated line cells in the central nervous system and thymus gland was observed.

Animals↗
PubMed1983

Autoimmune encephalomyelitis (EAE) mediated or prevented by T lymphocyte lines directed against diverse antigenic determinants of myelin basic protein. Vaccination is determinant specific.

Lines of T lymphocytes reactive against the basic protein of myelin (BP) were found in previous studies to mediate experimental autoimmune encephalomyelitis (EAE) in rats. Moreover, inoculation of rats with attenuated anti-BP line cells vaccinated them against subsequent attempts to induce active EAE by injection of BP in adjuvant. In the present study, we investigated the effects of T lymphocyte lines reactive to different antigenic determinants on the BP molecule, they are the major encephalitogenic peptide (EP) determinant present on guinea pig BP (G-BP), and minor, non-EP determinants present on bovine BP (B-BP). We found that both lines of T lymphocytes could mediate EAE. Resistance to active EAE acquired by spontaneous recovery from line mediated EAE or by vaccination with attenuated cells, however, was found to be specific for the particular BP determinant. Thus, EAE may be mediated by lines of T lymphocytes reactive to different determinants on the BP molecule, but the resistance to EAE acquired by exposure to line cells is determinant specific. This suggests that acquired resistance to EAE is directed by the receptor specificity of the autoimmune anti-BP T cells.

Animals↗
PubMedDate not supplied

Immunospecific inhibition of nerve conduction by T lymphocytes reactive to basic protein of myelin.

Experimental autoimmune encephalomyelitis (EAE) induced by immunization to the basic protein of central nervous system myelin (BP) is a paralytic disease in which T lymphocytes attack the individual's own central nervous system. As the target is in white matter, EAE has been considered an experimental model of some aspects of human disease such as multiple sclerosis. To investigate whether autoimmune T lymphocytes could produce paralysis, we studied the effects on the electrophysiology of isolated nerves produced by T-lymphocyte lines reactive specifically to BP or other antigens. We now report that propagation of action potentials evoked by electrical stimulation was blocked by incubating optic nerves with specific anti-BP T cells. This blockade could be reversed for up to two hours by removing the anti-BP line cells from the optic nerve. The anti-BP line cells had no effect on conduction along allogeneic optic nerves or syngeneic peripheral nerves. This indicates that disruption of the function of myelin in neuroimmunological disease may result from an immunologically specific interaction between autoimmune T lymphocytes and myelin antigens.

Action Potentials↗
PubMedDate not supplied

Listeria monocytogenes pericarditis in a chronically hemodialyzed patient.

We describe the third documented case of Listeria monocytogenes pericarditis. This occurred in a 54-year-old woman with end-stage renal failure on chronic hemodialysis. Her initial presentation was one of Listeria monocytogenes bacteremia, which apparently responded to two weeks of cefazolin sodium therapy. After cessation of therapy the patient returned with Listeria monocytogenes pericarditis, this responding completely to four weeks of erythromycin therapy. We could not rule out coexisting endocarditis, especially since we found high levels of circulating immune complexes which subsided as the patient's condition improved. Further immunological studies displayed a decrease in cellular functions. This case illustrates the importance of Listeria monocytogenes as a human pathogen in immunocompromised patients. Listeria should be included among the potential causative agents of pericarditis in such patients.

Erythromycin↗