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Biomedical subjects

N Talal

Publications and source records attributed to N Talal.

At least 217 records · Page 12Linked to original sources
PubMed1979

An evaluation of salivary scintigraphy in Sjögren's syndrome.

Sequential salivary scintigraphy, labial salivary gland biopsy, and measurement of stimulated parotid flow rate were performed in 50 patients suspected of having Sjögren's syndrome. The value of these tests in the diagnosis of this disease was compared. Salivary scintigraphy and labial salivary gland biopsy can be used together to diagnose the oral component of Sjögren's syndrome. Abnormal salivary scintigraphy correlated with both of the other tests and may be considered optional in the diagnostic evaluation.

Female↗
PubMed1979

Immunoblastic sarcoma with features of Sjögren's syndrome and systemic lupus erythematosus in a patient with immunoblastic lymphadenopathy.

A patient with immunoblastic lymphadenopathy and features of Sjögren's syndrome and systemic lupus erythematosus is presented. Clinical features included generalized lymphadenopathy, rash, alopecia, and synovitis, with associated laboratory abnormalities of a positive antinuclear factor and double-stranded DNA antibodies, positive lupus band test, and hemolytic anemia. Symptoms of Sjögren's syndrome included dry eyes and mouth and swollen parotid gland; biopsy results of the accessory salivary glands were positive. At autopsy immunoblastic sarcoma was found that involved the myocardium, which stained for both kappa and lambda light chains by immunoperoxidase techniques.

Aged↗
PubMed1979

Suppressor cells and immunodeficiency in (NZB x NZW)F1 hybrid mice.

Old (15-20 month) male (NZB x NZW)F1 (B/W) mice have severely impaired spleen cell reactivity to phytohemagglutinin (PHA), a mitogen which stimulates mainly T lymphocytes. Spleen cells from old mice markedly suppressed the PHA response of splenocytes from young (3-4 month) B/W males. Similar suppressor activity was not present in the spleens of old mice of four nonautoimmune strains. The suppressor activity of old B/W spleen cells was mediated by a nonphagocytic, radioresistant, mononuclear leukocyte. Although this cell was eluted in the "T lymphocyte" fraction of nylon wool colums, it was not sensitive to treatment with anti-Thy-1 antiserum and complement. Suppressor activity was lost after 18 h incubation at 37 degrees C in tissue culture medium. Supernatants of these overnight cultures had no suppressive effect on fresh young B/W spleen cells. Old B/W spleen cells suppressed PHA reactivity more than concanavalin A or lipopolysaccharide reactivity. Kinetic studies demonstrated an increasing suppression with time over 72 h of culture. This study demonstrate that the severely impaired PHA reactivity of old B/W mice is mediated, at least in part, by active suppression.

Aging↗
PubMed1979

Delayed androgen treatment prolongs survival in murine lupus.

Female NZB/NZW F1 mice were treated as adults with 5-alpha-dihydrotestosterone powder packed into subcutaneous implants. Two treatment protocols were followed: (a) 3-mo-old mice received 6 mg of androgen, and (b) 6-mo-old mice were castrated and given 12 mg of androgen. Sham females received empty implants. Mice were followed monthly for surival, for antibodies to DNA and polyadenylic acid, and for renal histopathology. The percent survival at 11 mo was 74% for mice treated at 3 mo, compared to 11% for the sham controls, and 100% for mice treated at 6 mo, compared to 20% for their sham controls. Androgen-treated mice had less immune complex glomerulonephritis as determined by immunofluorescent and electron microscopy. Surprisingly, treated mice had no significant sustained reduction in antibodies to DNA although they had reduced antibodies to polyadenylic acid. These results suggest that androgens can still prolong survival and reduce immune complex deposition even when treatment is delayed to an age when disease is relatively established. After delayed androgen treatment, mice survive despite the presence of high levels of IgG antibodies to DNA.

Animals↗
PubMed1979

Characteristics of peritoneal lymphocytes from New Zealand Black and normal mice autoreactive for mouse erythrocytes.

New Zealand Black mice spontaneously develop autoimmune hemolytic anemia. Peritoneal cavity lymphocytes from NZB mice include a high proportion of cells that bind autologous erythrocytes. These cells produce ani-erythrocyte antibody that can be demonstrated when target erythrocytes are treated with bromelin. Such autoreactive cells are also present in normal mice, though in much smaller numbers. Aging and sex influence the peritoneal anti-erythrocyte response to bromelin-treated mouse erythrocytes. Older mice generally produce more rosettes and plaques than younger animals, and females have higher responses than males. During short-term culture in the absence of antigen, the response to bromelin-treated mouse erythrocytes increases. By contrast, the response to untreated mouse erythrocytes decreases during the same culture conditions. The in vitro response to bromelin-treated mouse erythrocytes by New Zealand Black peritoneal lymphocytes is suppressed by a cell that binds to untreated erythrocytes. The enhanced response to bromelin-treated mouse erythrocytes in culture may reflect the loss of this suppressor cell.

Aging↗
PubMed1979

Natural killing in estrogen-treated mice responds poorly to poly I.C despite normal stimulation of circulating interferon.

Natural killing by mouse spleen cells can be stimulated in vivo by interferon or by agents that stimulate interferon, such as poly I.C. Natural killing can be suppressed in vivo by the sustained administration of 17 beta-estradiol. In BALB/c mice that had been treated with 17 beta-estradiol for 10 weeks, natural killing did not respond to intravenous poly I.C, although stimulation of circulating interferon was equal to controls. Estradiol, then, does not block interferon production but does suppress the response of natural killer cells to interferon. It is suggested that estrogens either block the maturation of natural killer cells or reduce the number of natural killer cell precursors.

Animals↗
PubMed1979

Failure of NZB spleen to respond to prethymic bone marrow suppressor cells.

Mouse bone marrow contains theta-negative lymphocytes that can suppress an in vitro plaque response by spleen cells primed in vivo with burro red blood cells (BRBC). These bone marrow cells are radiosensitive and can be induced with thymosin fraction 5 or alpha 1 thymic peptides to express the theta antigen. Enrichment for these suppressor pre-T lymphocytes can be achieved by a one-step density centrifugation, macrophage depletion, or a combination of both procedures. NZB mice, which spontaneously develop an autoimmune disorder, have a suppressor abnormality revealed by this assay system. Upon analysis, they have normal BM pre-T suppressor cells but their spleen cells are refractory to the BM suppressor signal. NZB BM suppressor cells inhibit the response by DBA/2 spleen cells, but DBA/2 BM suppressor cells do not inhibit NZB spleen. This resistance to suppression is a property of the B cell fraction recovered from NZB spleen.

Animals↗
PubMed1979

Characteristics of in vitro production of antibodies to DNA in normal and autoimmune mice.

The in vitro production of antibodies to dsDNA was studied with spleen cells from normal and autoimmune mice. After culture for 4 days, the binding of dsDNA in the culture supernatant was measured by a radioimmunoprecipitation assay. The production of antibodies to dsDNA by spleen cells appeared at 15 hr after culture and reached a plateau at 24 hr. No antibodies were produced by thymus cells or splenic T cells. The specificity for dsDNA was shown by competitive inhibition with nonradioactive nucleic acids. Autoimmune strains of mice (NZB/NZW, BXSB, MRL/1) produced more antibodies to dsDNA than did several control strains. Young B/W mice and control strain mice produced mainly IgM antibodies, whereas older B/W mice produced predominantly IgG antibodies to dsDNA. The in vitro production of antibodies to dsDNA by aged B/W spleen cells was macrophage and T cell dependent.

Animals↗
PubMed1979

Natural killer cells, bone, and the bone marrow: studies in estrogen-treated mice and in congenitally osteopetrotic (mi/mi) mice.

Mice lose natural killer cells after 6 weeks of treatment with 17 beta-estradiol. We here demonstrate that the same protocol leads to loss of genetic resistance to bone marrow transplantation and to significant osteoproliferation with loss of bone marrow. We also show that mice with reduced marrow because of congenital osteopetrosis are deficient in natural killing. These findings are consistent with previous evidence that natural killing and genetic resistance to bone marrow transplantation are dependent upon the marrow. Temporal studies of bone histology and radiology during and after treatment with estrogen reveal that alterations in natural killing proceed more rapidly than changes in bone marrow volume. These studies also demonstrate that estrogens induce osteoproliferation only at endosteal surfaces that are adjacent to hematopoietic marrow. From these observations, we conclude that estrogens do not reduce natural killer cells simply by reducing the volume of bone marrow. Estrogens may instead have an effect on bone marrow. Estrogens may instead have an effect on bone marrow cells that leads both to osteoproliferation and to a deficiency of marrow-dependent cells.

Animals↗
PubMed1979

Age-related changes in antibody-dependent cell-mediated cytotoxicity in mouse spleen.

The age-related variation in antibody-dependent cell-mediated cytotoxicity (ADCC) in spleen was examined in four different mouse strains (DBA/2, Balb/c, NZB and NZB/NZW). The ADCC effector activity against antibody-coated chicken red blood cells in untreated spleen from all four strains was roughly comparable. An initial rise in activity with increasing age until two to three months was followed by a sharp decline in effector activity. Treatment of the spleen cells with poly-l-lysine-coated carbonyl iron to remove phagocytes resulted in a decrease in ADCC activity in NZB, NZB/NZW and DBA/2 strains at all ages examined. The same general pattern of age-dependent decline was still seen in these depleted spleens. However, the same treatment essentially abolished ADCC in Balb/c spleen at all ages studied.

Age Factors↗
PubMed1978

Evidence that the malignant lymphoma of Sjögren's syndrome is a monoclonal B-cell neoplasm.

We studied the malignant lymphomas that developed in patients with Sjögren's syndrome and the antecedent benign salivary-gland lesions to determine their cellular characteristics. We used an immunoperoxidase technic that identified intracellular gamma, alpha and mu heavy chains and kappa and lambda light chains. In six of nine patients, the lymphomas were composed of cells containing intracytoplasmic immunoglobulin that was exclusively IgMK. The benign lymphoepithelial salivary-gland lesions preceding these malignant tumors consisted of approximately equal numbers of lymphoid cells containing either kappa or lambda light chains. Thus, in some patients with Sjögren's syndrome, there may be a progression in the lympho-proliferative lesions from a polyclonal infiltrate to a monoclonal neoplasm. Intracytoplasmic immunoglobulin identifies six of the nine cases as being B-cell in origin.

Aged↗
PubMed1978

Effect of castration and sex hormone treatment on survival, anti-nucleic acid antibodies, and glomerulonephritis in NZB/NZW F1 mice.

NZB/NZW F1 mice of both sexes were castrated at 2 wk of age and implanted subcutaneously with silastic tubes containing either 5-alpha-dihydrotestosterone or estradiol-17-beta. Mice receiving androgen showed improved survival, reduced anti-nucleic acid antibodies, or less evidence of glomerulonephritis as determined by light, immunofluorescent, and electron microscopy. By contrast, opposite effects were observed in castrated mice receiving estrogen. Intact male NZB/NZW F1 mice received androgen implants at 8 mo, an age when they develop an accelerated autoimmune disease associated with a decline in serum testosterone concentration. Such treated mice had improved survival and reduced concentrations of antibodies to DNA and to polyadenylic acid (Poly A). Prepubertal castration of male NZB/NZW F1 mice results in an earlier appearance of IgG antibodies to Poly A. This effect of castration was prevented if neonatal thymectomy was also performed.

Age Factors↗
PubMed1978

Monozygotic twins with Klinefelter's syndrome discordant for systemic lupus erythematosus and symptomatic myasthenia gravis.

Monozygotic twins with Klinefelter's syndrome were evaluated for two distinct illnesses. One subject had clinical and serologic evidence of systemic lupus erythematosus and no symptoms of muscle weakness. His identical twin had typical symptoms and laboratory evidence of myasthenia gravis. Antibodies to acetylcholine receptors were present in both subjects. These patients are discussed in relation to genetic, hormonal, and immunologic mechanisms involved in the pathogenesis of these two disorders.

Diseases in Twins↗
PubMed1978

Relationshipp of HLA-Dw3 and HLA-B8 to Sjögren's syndrome.

Nineteen patients with Sjögren's syndrome were evaluated for the presence of HLA-B8 and HLA-Dw3. HLA-B8 was found in 57.8% of patients and 20.1% of 96 controls (P less than 0.001). HLA-Dw3 was detected in 73.7% of the patients and 24.0% of controls (P less than 0.0001). Statistical evaluation of the association of both antigens with Sjögren's syndrome revealed that the primary association was with HLA-Dw3 (P less than 0.005). Patients with HLA-Dw3 had a lower mean parotid salivary flow rate (0.8 +/- 0.3 ml/10 minutes/gland versus 5.6 +/- 1.2 ml/10 minutes/gland, P less than 0.0004) and a more intense lymphocytic infiltration into labial salivary glands (focus score 7.2 +/- 0.9 versus 3.4 +/- 0.9, P less than 0.04) than did patients without HLA-Dw3. The difference in the intensity of the lymphocytic infiltration was even more significant when patients with both HLA-Dw3 and HLA-B8 were compared with patients with neither antigen (focus score 7.5 +/- 1.0 versus 2.8 +/- 0.8, P less than 0.02). In addition, all patients with severe keratoconjunctivitis sicca had both antigens. Our observations suggest that a number of genes may interact to determine susceptibility and severity in Sjögren's syndrome.

Adolescent↗
PubMed1978

The relationship of membrane antigens on 141 (NZB) and EL4 (C57BL) lymphoma cells as demonstrated by antibody-induced resistance to complement-mediated cytotoxicity.

We have studied the ability of various antisera to induce resistance to complement-dependent lysis (CdL) (lysostripping) of surface antigens of B and T lymphoma cells. Alloantisera, xenoantisera, as well as anti-Rauscher-leukemia virus (RLV) antisera, were used. Whereas all antisera could induce resistance to CdL mediated by the same serum that served for lysostripping (autolysostrip), only some of the tested antisera could induce resistance to CdL by other antisera (co-lysostrip). In some combinations co-lysostrip was unidirectional, i.e., in a pair of antisera, one induced autolysostrip as well as co-lysostrip, whereas the other antiserum induced autolysostrip only. In other combinations co-lysostrip was reciprocal. These investigations do not support the possibility that viral components and alloantigenic determinants are associated on mouse lymphoma cells.

Animals↗