A genetic lesion that arrests plasma cell homing to the bone marrow.
Proc Natl Acad Sci U S A
; 100(22): 12905-10, 2003 Oct 28.
Article
en En
| MEDLINE
| ID: mdl-14555759
ABSTRACT
The coordinated regulation of chemokine responsiveness plays a critical role in the development of humoral immunity. After antigen challenge and B cell activation, the emerging plasma cells (PCs) undergo CXCL12-induced chemotaxis to the bone marrow, where they produce Ab and persist. Here we show that PCs, but not B cells or T cells from lupus-prone NZM mice, are deficient in CXCL12-induced migration. PC unresponsiveness to CXCL12 results in a marked accumulation of PCs in the spleen of mice, and a concordant decrease in bone marrow PCs. Unlike normal mice, in NZM mice, a majority of the splenic PCs are long-lived. This deficiency is a consequence of the genetic interactions of multiple systemic lupus erythematosus susceptibility loci.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Células Plasmáticas
/
Células de la Médula Ósea
/
Receptores Mensajeros de Linfocitos
/
Quimiocinas CXC
Límite:
Animals
Idioma:
En
Revista:
Proc Natl Acad Sci U S A
Año:
2003
Tipo del documento:
Article
País de afiliación:
Estados Unidos