Reciprocal lymphoid cell homing studies using wild and LPR (lymphoproliferation) mutant C57BL mice.
The injection of lymphoid cells from adult lpr mice into normal and athymic congenic mice does not transfer the lpr (lymphoproliferation) syndrome. We studied whether this phenomenon could be due to abnormal homing. The lymphoid cells from lpr donors do not show a marked deficiency of migration to lymphoid organs in comparison with cells from Wild donors and a T-cell lymphoma BL/VL3. The lymphoid organs of lpr recipients do not show an intrinsic abnormality as homing sites for lymphoid cells. The data reveal some minor migration preferences: the lpr cells migrate better than Wild cells into lpr lymph nodes (including athymic lpr hosts), whereas Wild cells migrate slightly better than lpr cells into Wild lymph nodes. In spite of such minor preferences, Wild cells can efficiently migrate into lpr lymphoid organs, as well as lpr cells into Wild lymphoid organs. Thus, the lack of transfer of lymphadenopathy in Wild recipients cannot be attributed to an alteration of lpr cell homing.
Rodriguez
E M
EM
Department of Radioprotection, SCK/CEN MOL, Belgium.
Hooghe
R J
RJ
Loor
F
F
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D002465:Cell Movement / Q000235:genetics; D007116:Immunization, Passive; D008198:Lymph Nodes / Q000473:pathology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000276:immunology / Q000473:pathology / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009928:Organ Specificity; D013577:Syndrome; D016176:T-Lymphocyte Subsets / Q000473:pathology