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Biomedical subjects

N Talal

Publications and source records attributed to N Talal.

At least 325 records · Page 18Linked to original sources
PubMed1969

Rapid loss of tolerance induced in weanling NZB and B-W F1 mice.

Young adult mice (30 to 43 days old) of autoimmune NZB and BIW F(1) strains failed to develop immunologic tolerance when treated with ultracentrifuged bovine gamma globulin and then challenged 12 days later. By contrast, weanling NZB and B/ W F(1) mice (18 to 25 days) as well as weanling C3H mice (16 to 19 days) became tolerant and had no serum antibody 12 days after challenge. The C3H mice remained unresponsive, but NZB and B! W F(1) mice produced antibody between days 27 and 41. The rapid loss of previously established tolerance to foreign antigens could have its parallel in the loss of tolerance to autoantigens with subsequent development of lupus nephritis and Coombs' positive hemolytic anemia in these animals.

Anemia, Hemolytic, Autoimmune↗
PubMed1969

Relative inability to induce tolerance in adult NZB and NZB-NZW F1 mice.

Immunologic tolerance to ultracentrifuged bovine gamma globulin could not be induced in 6-wk old NZB or B/W mice, but developed readily in C3H, NZW, and C57Bl mice. NZB and B/W mice, as well as Balb/c mice, failed to become tolerant to ultracentrifuged human gamma globulin. The NZB and B/W mice also showed higher antibody titers to a standard antigenic challenge. This immunologic hyperreactivity and lack of experimental tolerance may be related to the lack of self-tolerance, autoimmunity, and lymphomas that develop in these mice at a later age.

Animals↗
PubMed1969

The pathogenesis of autoimmunity in New Zealand mice, I. Induction of antinucleic acid antibodies by polyinosinic-polycytidylic acid.

Antibodies to DNA and RNA were induced in young NZB/NZW F(1) (B/W) female mice following multiple injections of the interferon-inducer polyinosinic.polycytidylic acid (poly I.poly C). Despite serum concentrations of interferon adequate to inhibit the C-type murine leukemia viruses, there was an acceleration of the autoimmune disease in these animals. Anti-RNA, but not anti-DNA antibodies, were induced in B/W male mice, as well as in NZB and NZW mice. Anti-RNA antibodies were also found in 50 per cent of female B/W mice who had never received poly I.poly C and in 8 of 24 sera from patients with systemic lupus erythematosus. These results suggest that double-stranded RNA functions as a potent antigen in New Zealand mice. Naturally occurring nucleic acids (e.g., viruses) probably act as stimuli to a genetically hyperreactive immune system. According to this hypothesis, the unusual feature in this disease is not a unique virus, but rather the unique genetic susceptibility of the B/W (particularly female) host to immunization with nucleic acids. A similar pathogenetic mechanism may be operative in some humans with systemic lupus erythematosus.

Animals↗
PubMed1967

Impaired Lymphocyte Transformation and Delayed Hypersensitivity in Sjögren's Syndrome.

In vitro lymphocyte transformation in response to phytohemagglutinin and streptolysin O and in vivo skin sensitization to 2,4-dinitrochloro-benzene has been studied in patients with Sjögren's syndrome and in normal controls of comparable age and sex. Both the in vivo and in vitro responses were significantly impaired in the Sjögren's patients as compared to the controls. This lack of response to mitogenic agents is probably due to an intrinsic defect in the lymphocytes rather than to a serum factor. The abnormalities were less marked in patients whose disease was localized to the parotid and lacrimal glands than in those with generalized disease, i.e., with complicating rheumatoid arthritis or pseudolymphoma.

Journal Article↗