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Characterization of human T8+ suppressor and contrasuppressor cells, separated by the lectin <em>Vicia villosa</em>.
- Source :
- Immunology; Feb88, Vol. 63 Issue 2, p247-254, 8p
- Publication Year :
- 1988
-
Abstract
- The helper function of human T4<superscript>+</superscript> cells acting on autologous B cells, in the presence of monocytce-enriched cells (MEC), has been studied using the hapten--carrier conjugate DNP--streptococcal antigen (DNP-SA). The antibody response can be suppressed by T8<superscript>+</superscript> cells, but selection of a Vicia villosa lectin-non-adherent (T8VV<superscript>-</superscript>) subset enhances the suppresor function. The T8 Vicia villosa lectin-adherent (T8VV<superscript>+</superscript>) cells are not suppressive, rather they inhibit the T8VV<superscript>-</superscript> cell suppressor function. Sequential reconstitution studies suggest that the target of both T8VV<superscript>-</superscript> suppressor-cell and T8VV<superscript>+</superscript> contrasuppressor activity is the T4 helper-inducer cell. This was established after the separation of T4<superscript>+</superscript> cells into Leu 8<superscript>-</superscript> helper- and Leu 8<superscript>+</superscript> suppressor-inducer cells. Activation of T8VV<superscript>-</superscript> and T8VV<superscript>+</superscript> cells with antigen before reconstitution with fresh lymphocytes and MEC suggests that T8VV<superscript>-</superscript> suppressor activity is antigen specific, whereas T8VV<superscript>+</superscript> cell contrasuppressor function is non-specific. We suggest that the human T8<superscript>+</superscript> cells are functionally heterogeneous and consist not only of suppressor and cytotoxic cells but also contrasuppressor cells. [ABSTRACT FROM AUTHOR]
- Subjects :
- B cells
MONOCYTES
ANTIGENS
LYMPHOCYTES
CELLS
LEUCOCYTES
LECTINS
Subjects
Details
- Language :
- English
- ISSN :
- 00192805
- Volume :
- 63
- Issue :
- 2
- Database :
- Complementary Index
- Journal :
- Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 14011534