Phenotypic and functional properties of γδ T Cells from patients with Guillain Barre syndrome

被引:17
作者
Borsellino, G
Poccia, F
Placido, R
Tramonti, D
Mancino, G
Luchetti, S
Galgani, S
Bonetti, B
Bach, S
Cipriani, B
Brosnan, CF
Battistini, L
机构
[1] IRCCS Santa Lucia, Lab Neuroimmunol, I-00179 Rome, Italy
[2] IRCCS L Spallanzani, Int Ctr AIDS & Emerging Infect, I-00149 Rome, Italy
[3] Osped S Camillo Roma, Dept Neurosci Lancisi, Rome, Italy
[4] Univ Verona, Dept Neurol, I-37100 Verona, Italy
[5] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 USA
关键词
Guillain Barre syndrome; gamma-delta T cells; cytokines;
D O I
10.1016/S0165-5728(99)00165-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In this study we have examined the phenotypic and functional properties of circulating gamma delta T cells in patients with Guillain Barre syndrome (GBS), in normal healthy controls, and in patients with active multiple sclerosis (MS). Cells expressing the V delta 2 T cell receptor showed elevated expression of the C-lectin receptor NKRP1A in both GBS and MS, suggestive of an activated state. However, in patients with GBS these cells failed to respond to pyrenil-pyrophosphate derivatives and V delta 2 + T cell clones derived from these patients released lower levels of IFN gamma than V delta 2 + clones derived from controls and MS patients. In contrast, in patients with GBS the V delta 1 + subset was expanded, showed elevated expression of NKRP1A and V delta 1 + clones derived from these patients secreted high levels of IL-4. Our findings of expanded NKRP-1A +, IL-4-producing V delta 1 T cells in the GBS patients suggests the possibility that these cells are activated by the recognition of non-protein antigens in an MHC-unrestricted manner and contribute to the humoral response to glycolipids that is a hallmark of this disease. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:199 / 207
页数:9
相关论文
共 54 条
[31]   T-LYMPHOCYTE RECOGNITION SITES ON PERIPHERAL-NERVE MYELIN P-0 PROTEIN [J].
PETTE, M ;
LININGTON, C ;
GENGAROLI, C ;
GROSSEWILDE, H ;
TOYKA, KV ;
HARTUNG, HP .
JOURNAL OF NEUROIMMUNOLOGY, 1994, 54 (1-2) :29-34
[32]  
Poccia F, 1996, J IMMUNOL, V157, P449
[33]  
Poccia F, 1997, J IMMUNOL, V159, P6009
[34]  
Poggi A, 1999, J IMMUNOL, V162, P4349
[35]   ACTIVATED T-CELLS OF NONNEURAL SPECIFICITY OPEN THE BLOOD-NERVE BARRIER TO CIRCULATING ANTIBODY [J].
POLLARD, JD ;
WESTLAND, KW ;
HARVEY, GK ;
JUNG, S ;
BONNER, J ;
SPIES, JM ;
TOYKA, KV ;
HARTUNG, HP .
ANNALS OF NEUROLOGY, 1995, 37 (04) :467-475
[36]   CAMPYLOBACTER-JEJUNI INFECTION AND GUILLAIN-BARRE-SYNDROME [J].
REES, JH ;
SOUDAIN, SE ;
GREGSON, NA ;
HUGHES, RAC .
NEW ENGLAND JOURNAL OF MEDICINE, 1995, 333 (21) :1374-1379
[37]   ANTIGANGLIOSIDE GM(1) ANTIBODIES IN GUILLAIN-BARRE-SYNDROME AND THEIR RELATIONSHIP TO CAMPYLOBACTER-JEJUNI INFECTION [J].
REES, JH ;
GREGSON, NA ;
HUGHES, RAC .
ANNALS OF NEUROLOGY, 1995, 38 (05) :809-816
[38]   Human NK cells: Their ligands, receptors and functions [J].
Reyburn, H ;
Mandelboim, O ;
ValesGomez, M ;
Sheu, EG ;
Pazmany, L ;
Davis, DM ;
Strominger, JL .
IMMUNOLOGICAL REVIEWS, 1997, 155 :119-125
[39]   The immunopathology of Guillain-Barre syndrome [J].
Saida, K .
CURRENT OPINION IN NEUROLOGY, 1996, 9 (05) :329-333
[40]   Treatment of Guillain-Barre syndrome with intravenous immunoglobulin [J].
Sater, RA ;
Rostami, AM .
NEUROLOGY, 1998, 51 (06) :S9-S15