Phenotypic and functional characterization of T cell clones derived from the cerebrospinal fluid of multiple sclerosis patients
We describe here T cell cultures and clones established from the cerebrospinal fluid (CSF) of three patients with multiple sclerosis (MS) and one chronic meningitis patient with pleocytosis. Most of the cultures were activated with phytohemagglutinin (PHA) before growth in mitogen-free interleukin 2...
Gespeichert in:
Veröffentlicht in: | The Journal of immunology (1950) 1984-05, Vol.132 (5), p.2386-2392 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | We describe here T cell cultures and clones established from the cerebrospinal fluid (CSF) of three patients with multiple sclerosis (MS) and one chronic meningitis patient with pleocytosis. Most of the cultures were activated with phytohemagglutinin (PHA) before growth in mitogen-free interleukin 2 (IL 2), and were never restimulated. Some of the clones obtained have been propagated for over 1 yr and are strictly IL 2-dependent. Immunofluorescence analysis performed with various monoclonal antibodies revealed that the CSF-derived lines had the characteristics of activated T cells with a stable expression of either suppressor/cytotoxic or helper/inducer surface antigens. Most of the clones established had a predominantly suppressor phenotype (OKT8+), except for the clones derived from one MS patient, which expressed only the helper phenotype (anti-Leu-3a+). Consistent with these data, the CSF-derived cultures displayed a variety of immunoregulatory functions, such as the ability to lyse nonspecific and PHA-stimulated target cells, to produce IL 2 upon mitogenic activation, and to modulate polyclonally induced Ig responses. The availability of long-term CSF T cell cultures derived from MS patients at various disease stages might provide a useful tool in investigating the factor(s) involved in the etio-pathogenesis of the disease. |
---|---|
ISSN: | 0022-1767 1550-6606 |
DOI: | 10.4049/jimmunol.132.5.2386 |