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2+ TCR
+ T Lymphocytes from Healthy Donors and Multiple Sclerosis Patients1
*
Laboratorio Immunopatologia, Istituto Nazionale per la Ricerca sul Cancro e Centro Biotecnologie Avanzate (IST-CBA), Genoa, Italy;
Laboratorio Immunologia dei Tumori, Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele, Milan, Italy;
Laboratorio Neuroimmunologia, Istituto di Ricovero e Cura a Carattere Scientifico Santa Lucia, Rome, Italy;
§
Dipartimento di Neuroscienze "Lancisi," Ospedale S. Camillo, Rome, Italy;
¶
Dipartimento di Scienze Neurologiche, Universita’ "La Sapienza," Rome, Italy; and
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Department of Pathology, Albert Einstein College of Medicine, Bronx, NY
T lymphocytes are thought to play a role in the pathogenesis
of multiple sclerosis (MS) contributing to demyelinization and fibrosis
in the central nervous system. In this study, we show that, in MS
patients with active disease, the percentage of circulating
V2+ T cells coexpressing NKRP1A is significantly
increased compared with healthy donors. V2+ and
V1+ T cells were sorted from MS patients and healthy
volunteers and cloned. At variance with V1+ clones, all
V2+ clones expressed NKRP1A, which was strongly
up-regulated upon culture with IL-12; this effect was neutralized by
specific anti-IL-12 Abs. No up-regulation of NKRP1A by IL-12 was
noted on V1+ clones. RNase protection assay showed that
IL-12R ß2 subunit transcript was significantly less represented in
V1+ than V2+ clones. This finding may
explain the different effect exerted by IL-12 on these clones. In
transendothelial migration assays, V2+
NKRP1A+ clones migrated more effectively than
V1+ clones, and this migratory potential was enhanced
following culture with IL-12. Migration was strongly inhibited by the
F(ab')2 of an anti-NKRP1A Ab, suggesting that this
lectin is involved in the migration process. We also show that, in
freshly isolated PBMC from MS patients, the migrated population was
enriched for V2+ NKRP1A+ cells. We conclude
that the expression of NKRP1A on V2+ cells is associated
with increased ability to migrate across the vascular endothelium and
that this phenomenon may be regulated by IL-12 present in the
microenvironment.
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