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Lactoferrin Triggers In Vitro Proliferation of T Cells of Lewis Rats Submitted to Mycobacteria‐Induced Adjuvant Arthritis
Author(s) -
ESAGUY N.,
FREIRE O.,
EMBDEN J. D. A.,
ÁGUAS A. P.
Publication year - 1993
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1993.tb01706.x
Subject(s) - antigen , in vitro , immunology , arthritis , adjuvant , t cell , lymph node , spleen , medicine , chemistry , immune system , biochemistry
We have recently reported antigenic (B‐ccll) cross‐reactivity between the mycobacterial 65 kDa heat shock protein (hsp65) and human lactoferrin (LF) and we suggested that this cross‐reactivity might have a role in mycobacteria‐associated autoimmune disease. Here, we have searched for anti‐LFT‐cell reactivity in Lewis rats submitted to a mycobacteria‐triggered autoaggressive disorder (adjuvant arthritis, A A), an autoimmune disorder characterized by high anti‐hsp65 reactivity. We have quantified the in vitro proliferate response to LF of lymph node and spleen cells of Lewis rats killed 9, 14 and 21 days after the immunization with the AA‐triggering, mycobacteria‐containing adjuvant (complete Freund's adjuvant. CFA). We found that LF induced significant proliferation of lymph node T cells of rats undergoing AA. This T‐cell proliferation was not as marked as the one provoked by hsp65; it was, nevertheless, significantly higher ( P < 0.05) than that produced by a non‐arthritogenic antigen (i.e. albumin). T cells from naive or mineral oil (incomplete Frcund's adjuvant, IFA) injected rats did not respond to LF or hsp65. These data indicate that LF may work as an accessory stimulatory factor of the T‐cell autoreactivity associated with mycobacteria‐induced arthritis.
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