Marked depletion at the late pro-B cell stage in the bone marrow of lpr mice correlates with the development of lymphadenopathy but not autoimmunity.
Eur J Immunol
; 26(9): 2087-92, 1996 Sep.
Article
en En
| MEDLINE
| ID: mdl-8814251
We have found that old lpr mice exhibit a loss of mature B cells in the bone marrow. The deleted population is HSAlo B220hi and is generated from the peripheral pool. Abnormalities in the microenvironment could explain the absence of mature B cells. Thus, old lpr bones were grafted under the skin of normal adult Ly5.1 hosts and examined 3 weeks later for the presence of Ly5.1+ B220hi cells. Our data show that the lpr medullary compartment was efficiently restored by host B cells. These results suggest that the bone marrow microenvironment of old lpr mice is able to sustain mature B cells. However, transfer of T cell-depleted bone marrow cells from old lpr mice to Rag-2 -/- mice leads to incomplete and inefficient repopulation of the host medullary compartment. Thus, a defect at an early stage of B cell differentiation was detected: using four-color flow cytometry, we found a profound depletion of the late pro-B B220+ CD43+ HSA+ BP-1+ cell population in aging lpr mice. This depletion was not observed in old autoimmune-prone MRL-+/+ mice which develop only autoantibodies but was present in B6-lpr mice which develop a lymphadenopathy and an indolent autoimmune syndrome. Altogether, our results demonstrate an age-linked defect in the progression of B cell differentiation in lpr mice independent of the presence of autoantibodies and targeted to the late pro-B cell subset.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Células de la Médula Ósea
/
Células Madre Hematopoyéticas
/
Linfocitos B
/
Autoinmunidad
/
Enfermedades Linfáticas
/
Trastornos Linfoproliferativos
Límite:
Animals
Idioma:
En
Revista:
Eur J Immunol
Año:
1996
Tipo del documento:
Article
País de afiliación:
Francia
Pais de publicación:
Alemania