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Biomedical subjects

A Schuler

Publications and source records attributed to A Schuler.

48 records · Page 3Linked to original sources
PubMed1986

Rearrangement of antigen receptor genes is defective in mice with severe combined immune deficiency.

A process unique to lymphocyte differentiation is the rearrangement of genes encoding antigen-specific receptors on B and T cells. A mouse mutant (C.B-17scid) with severe combined immune deficiency, i.e., that lacks functional B and T cells, shows no evidence of such gene rearrangements. However, rearrangements were detected in Abelson murine leukemia virus-transformed bone marrow cells and in spontaneous thymic lymphomas from C.B-17scid mice. Most of these rearrangements were abnormal: approximately 80% of Igh rearrangements deleted the entire Jh region, and approximately 60% of TCR beta rearrangements deleted the entire J beta 2 region. The deletions appeared to result from faulty D-to-J recombination. No such abnormal rearrangements were detected in transformed tissues from control mice. The scid mutation may adversely affect the recombinase system catalyzing the assembly of antigen receptor genes in developing B and T lymphocytes.

Abelson murine leukemia virus↗
PubMed1984

Immune response against the T-independent antigen alpha (1----3) dextran. II. Occurrence of B gamma memory cells in the course of immunization with the native polysaccharide is T cell dependent.

The immune response of BALB/c mice against the bacterial antigen dextran B1355S [alpha (1----3)dextran] (Dex), a class 2 T cell-independent antigen, is largely restricted to IgM class antibody production. However, despite the fact that Dex fails to give rise to enhanced IgG responses upon repeated immunization, the development of Dex-specific B gamma memory cells, i.e. resting B cells committed to the production of specific IgG antibodies, is observed upon immunization with Dex. These B gamma memory cells, albeit not activated to IgG production in situ, can be activated upon adoptive transfer into irradiated congenic BALB Ighb mice. This mouse strain is a nonresponder strain to Dex. The expression of adoptively transferred Dex-specific B gamma memory cells is T cell-independent as T cell depletion of spleen prior to cell transfer into BALB.Ighb recipients does not abolish the IgG response. Dex-primed athymic BALB/c nude mice, in contrast to euthymic mice, give a pronounced primary IgG response but do not develop Dex-specific B gamma memory cells. Yet, they do so when reconstituted with syngenic T cells prior to immunization. This indicates that the formation of Dex-specific B gamma memory cells requires the presence of functional T cells. The pronounced primary IgG anti-Dex response of nude mice is greatly impaired by T cell reconstitution. Thus, with regard to T cell dependence, there is an inverse relationship between the formation of B gamma memory cells and the capacity to produce IgG anti-Dex. Dex-specific B gamma memory cells from BALB/c mice are expressed in congenic BALB.Ighb recipients (nonresponder to Dex) but not when transferred into identically treated syngenic hosts. This also applies to memory cells from Dex-primed female (CBA/N X BALB/c)F1 [NBF1] or from (BALB/c X CBA/N)F1 hybrids. Dex-specific B gamma memory cells from these donors are demonstrable upon adoptive transfer into BALB.Ighb mice, but they are not expressed when transferred into syngenic recipients, including male NBF1 hybrids. NBF1 males, albeit possessing the VH-Dex+ allele, do not mount humoral responses to Dex, a deficiency which is ascribed to an X chromosome-linked B cell defect. The apparent absence of Dex-specific antibodies in NBF1 males provides an opportunity to examine whether B gamma memory cell expression is inhibited in syngenic recipients by anti-Dex or autologous anti-idiotype antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Elevated muscle tissue oxygen tension in short-term insulin-dependent diabetes mellitus.

In order to assess hemodynamic changes in early phases of insulin-dependent diabetes mellitus, muscle tissue oxygen tensions were determined in 7 newly diagnosed insulin-dependent diabetic patients and in 6 healthy control subjects matched for sex, age and weight. Muscle tissue oxygen tension was measured by polarrographic needle probes while breathing ambient air and oxygen enriched air with an oxygen concentration of 40 per cent as well. Three times during the experiment, heart rates, blood pressures, blood glucose concentrations, and capillary oxygen tensions were obtained. Heart rate, blood pressure, peripheral and autonomic nerve functions did not differ between the 2 groups studied. While breathing ambient air, muscle tissue oxygen tensions were significantly (p = 0.025) higher in the diabetic patients than in the control subjects. In contrast to the control subjects, diabetic patients did not increase muscle tissue oxygen tensions after inhalation of oxygen enriched air despite of an equal increase in capillary oxygen tensions (2p less than 0.05). Local tissue hypoxia does not seem to be a leading cause of hemodynamic abnormalities in the early phases of diabetes.

Adult↗
PubMedDate not supplied

Perihepatic lymphadenopathy: a marker of response to interferon alpha in chronic hepatitis C.

BACKGROUND/AIMS: Recently it was shown that perihepatic lymphadenopathy (PHL) correlates with histological activity in chronic hepatitis C. However, the question whether there is a correlation between the response to interferon alpha and PHL has not yet been raised. METHODOLOGY: We examined 103 patients who had been treated with interferon alpha for hepatitis C. Prior to treatment all patients had undergone high resolution ultrasonography. Thirty-six patients had follow up ultrasound scans during the course of the treatment. According to size and number of lymph nodes we introduced a grading of the PHL and determined grade I as minimal, grade II as medium and grade III as extensive PHL. RESULTS: Classification of PHL prior to treatment revealed 40 patients with PHL I, 30 with grade II and 33 with grade III. Hepatic inflammatory activity according to the Ishak score was increased in patients with PHL III (9.1+/-2.4) compared to PHL II (6.7+/-2.9) and PHL I (7.3+/-3.1) (p=0.01). In patients with PHL grade I prior to treatment 45% were initial responder, patients with grade II or III showed response rates of 40% and 33%, respectively. During therapy we found an increase of PHL in one out of 13 primary responder vs. 10 out of 23 non-responder (p=0.03). CONCLUSIONS: In conclusion, monitoring of PHL by abdominal ultrasonography is a simple, non-invasive and cheap additional marker of response to interferon alpha.

Adolescent↗