Absence of an antigen-specific helper T cell required for the expression of the T 15 idiotype in mice treated with anti-mu antibody.
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Biomedical subjects
K Bottomly
Publications and source records attributed to K Bottomly.
Ly 9, an alloantigenic marker of lymphocyte differentiation.
A new lymphocyte cell surface alloantigen, provisionally designated Ly 9, is detected by flow microfluorometry(FMF), as an extra specificity in sera from anti-Lyt immunizations. Ly 9.2, one of the allelic specificities, commonly is detected as a unique immunofluorescence profile of thymocytes with anti-Lyt 3.1 sera. The alternative antigenic specificity, Ly 9.1, can be detected routinely in antisera prepared against Lyt 2.1 and Lyt 3.2. This lymphocyte alloantigen has both a unique strain and cell/tissue distribution. Quantitative measurement of Ly 9 immunofluorescence by FMF on heterozygote cells shows that Ly 9 antigen expression is co-dominant and reduced in levels relative to parental homozygote cells. Ly 9 is expressed on all thymocytes, peripheral lymphocytes, and on a subpopulation of cells in the bone marrow. This antigen is not expressed to any significant degree on erythrocytes, epidermal cells, sperm, or in suspensions of testis, brain, kidney, liver, or lung. FMF analysis and absorption typing reveals a quantitatively lower level of antigen expression on thymocytes compared with spleen or lymph node cells. Cytotoxic elimination experiments confirm that Ly 9 is expressed on at least 2 different T cell functional subsets and B cells.
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Fusiform erythrocytes resembling sickle cells in angora goats: observations on osmotic and mechanical fragilities and reversal of cell shape during anaemia.
Osmotic and mechanical fragilities of erythrocytes were determined for seven goats having 3.4-71 per cent fusiform erythrocytes. The osmotic fragility was related to the erythrocyte shape in that the osmotic resistance was considerably higher for bloods containing more than 26 per cent fusiform erythrocytes. A decrease in the proportion of fusiform erythrocytes in the same goats was related to an increase in the osmotic fragility. Anaemia was induced in two goats by removal of 200-400 ml of blood at three or four day intervals for eight weeks. Red cell values decreased by 28-43 per cent within three weeks, but further bleeding produced either no or less (0-21 per cent) reductions in these values. Slight reticulocytosis was seen during the anaemic phase and there was a concomitant increase in the mean corpuscular volume and mean corpuscular haemoglobin values. Reticulocytosis diminished before the start of recovery from anaemia and disappeared during the recovery phase. The most significant finding was the change in the erythrocyte morphology during production of and recovery from anaemia. The development of anaemia was associated with a gradual reduction in the proportion of fusiform erythrocytes or discoid cells and simultaneous increase in the proportion of erythrocytes exhibiting distinct poikilocytosis. Recovery from the anaemia was rapid (within five weeks), but reversal of the erythrocyte shape took several months. Severe blood loss anaemia in the goat is known to induce synthesis of haemoglobin C, and in these anaemic goats formation of a new haemoglobin, most likely haemoglobin C, was demonstrated by electrophoretic and column chromatographic analyses. It was concluded that the formation of haemoglobin C was responsible for the morphological changes in the erythrocytes.
Anemia↗
Mice whose B cells cannot produce the T15 idiotype also lack an antigen-specific helper T cell required for T15 expression.
The X-linked CBA/N defect in B cell function precludes an antibody response to phosphorylcholine (PC). Accordingly, (CBA/N X BALB/c)F1 male mice are unresponsive to PC and lack circulating immunoglobulin bearing the T15 idiotype characteristic of BALB/C anti-PC antibody. In contrast, (CBA/N X BALB/c)F1 female mice respond to PC and greater than 80% of the anti-PC antibody is T15+. No T-cell abnormalities are known to be associated with the CBA/N mutation. These experiments compared the ability of helper T cells from either (CBA/N X BALB/c)F1 male (T15-) or F1 female (T15+) mice to help F1 female B cells respond to PC and to influence the level of T15 expression. The results indicate that although F1 male T cells collaborated with F1 female B cells just as efficiently as F1 female T cells for the total anti-PC response, the percentage of T15 expression induced by F1 male T cells fell dramatically. The (CBA/N X BALB/c)F1 male thus appear to lack a helper T-cell subset required for dominant idiotype production. This helper T cell defect could be repaired by adding F1 female T cells primed to a second carrier to F1 male T cells and restimulating the cell mixture with PC coupled to the antigen used to prime the F1 male cells plus free second carrier. This result implies that conventional helper T cells derived from the F1 male donor can collaborate with a distinct helper T-cell subset from the F1 female donor which recognizes both carrier and idiotype to induce an anti-PC antibody response dominated by the T15 clonotype.
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Anti-idiotype induced regulation of helper cell function for the response to phosphorylcholine in adult BALB/c mice.
An adoptive secondary antibody response to phosphorylcholine (PC) can be generated by the transfer of keyhole limpet hemocyanin (KLH)-primed T cells, PC-bovine gamma globulin-primed B cells, and PC-KLH into irradiated syngeneic BALB/c mice. If the KLH-primed T-cell donors were pretreated with anti-idiotype antibodies directed against the BALB/c PC-binding myeloma TEPC 15, their T cells were unable to collaborate effectively with PC-primed B cells; moreover, they could suppress the helper activity of T cells from normal mice for the PC-KLH response. The Ly phenotype of these T cells was found to be Ly 1-, 2+. The specificity of the suppressor T-cell population induced by anti-T15 treatment appears to be both for idiotype (hapten) and carrier, since the suppressor T cells fail to interfere with the antibody response to PC on a heterologous carrier, nor do they suppress the response to trinitrophenol-KLH.
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