Abstract
Among human CD4+ T lymphocytes, 5-20% express the C-type lectin molecule NKRP1A. Interestingly, CD4+ NKRP1A+ T lymphocytes express high levels of β1 and β2 integrins, thus representing a T lymphocyte subset that can possibly adhere and migrate through vascular endothelium. Indeed, resting CD4+ NKRP1A+ lymphocytes, differently from the CD4+ NKRP1A- subset, migrated across endothelial cell monolayers in a Transwell chamber system. This transendothelial migration was strongly reduced after pre-treatment with an anti-NKRP1A monoclonal antibody (mAb). In addition, the NKRP1A negative Jurkatt CD4+ T-cell line that had been stably transfected with NKRP1A cDNA, migrated more rapidly and efficiently than untransfected Jurkatt cells. Finally, mAb-mediated cross-linking of NKRP1A molecule in CD4+ T lymphocytes induced the upregulation of the LFA1 Mg2+ binding site as well as β1 and β2 integrin chains. Altogether, these findings indicate that NKRP1A molecule is involved in transendothelial migration of resting CD4+ T lymphocytes.
| Original language | English |
|---|---|
| Pages (from-to) | 121-123 |
| Number of pages | 3 |
| Journal | Immunology Letters |
| Volume | 57 |
| Issue number | 1-3 |
| DOIs | |
| Publication status | Published - 1997 |
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Keywords
- Integrins
- Lectins
- Lymphocyte migration
- NKRP1A
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
Cite this
NKRP1A molecule is involved in transendothelial migration of CD4+ human T lymphocytes. / Poggi, Alessandro; Costa, Paola; Zocchi, Maria Raffaella; Moretta, Lorenzo.
In: Immunology Letters, Vol. 57, No. 1-3, 1997, p. 121-123.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - NKRP1A molecule is involved in transendothelial migration of CD4+ human T lymphocytes
AU - Poggi, Alessandro
AU - Costa, Paola
AU - Zocchi, Maria Raffaella
AU - Moretta, Lorenzo
PY - 1997
Y1 - 1997
N2 - Among human CD4+ T lymphocytes, 5-20% express the C-type lectin molecule NKRP1A. Interestingly, CD4+ NKRP1A+ T lymphocytes express high levels of β1 and β2 integrins, thus representing a T lymphocyte subset that can possibly adhere and migrate through vascular endothelium. Indeed, resting CD4+ NKRP1A+ lymphocytes, differently from the CD4+ NKRP1A- subset, migrated across endothelial cell monolayers in a Transwell chamber system. This transendothelial migration was strongly reduced after pre-treatment with an anti-NKRP1A monoclonal antibody (mAb). In addition, the NKRP1A negative Jurkatt CD4+ T-cell line that had been stably transfected with NKRP1A cDNA, migrated more rapidly and efficiently than untransfected Jurkatt cells. Finally, mAb-mediated cross-linking of NKRP1A molecule in CD4+ T lymphocytes induced the upregulation of the LFA1 Mg2+ binding site as well as β1 and β2 integrin chains. Altogether, these findings indicate that NKRP1A molecule is involved in transendothelial migration of resting CD4+ T lymphocytes.
AB - Among human CD4+ T lymphocytes, 5-20% express the C-type lectin molecule NKRP1A. Interestingly, CD4+ NKRP1A+ T lymphocytes express high levels of β1 and β2 integrins, thus representing a T lymphocyte subset that can possibly adhere and migrate through vascular endothelium. Indeed, resting CD4+ NKRP1A+ lymphocytes, differently from the CD4+ NKRP1A- subset, migrated across endothelial cell monolayers in a Transwell chamber system. This transendothelial migration was strongly reduced after pre-treatment with an anti-NKRP1A monoclonal antibody (mAb). In addition, the NKRP1A negative Jurkatt CD4+ T-cell line that had been stably transfected with NKRP1A cDNA, migrated more rapidly and efficiently than untransfected Jurkatt cells. Finally, mAb-mediated cross-linking of NKRP1A molecule in CD4+ T lymphocytes induced the upregulation of the LFA1 Mg2+ binding site as well as β1 and β2 integrin chains. Altogether, these findings indicate that NKRP1A molecule is involved in transendothelial migration of resting CD4+ T lymphocytes.
KW - Integrins
KW - Lectins
KW - Lymphocyte migration
KW - NKRP1A
UR - http://www.scopus.com/inward/record.url?scp=0030756833&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030756833&partnerID=8YFLogxK
U2 - 10.1016/S0165-2478(97)00050-3
DO - 10.1016/S0165-2478(97)00050-3
M3 - Article
VL - 57
SP - 121
EP - 123
JO - Immunology Letters
JF - Immunology Letters
SN - 0165-2478
IS - 1-3
ER -