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T Cells from Children with IDDM are Sensitized to Bovine Serum Albumin
Author(s) -
CHEUNG R.,
KARJALAINEN J.,
VANDERMEULEN J.,
SINGAL D. P.,
DOSCH H.M.
Publication year - 1994
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.1365-3083.1994.tb03514.x
Subject(s) - bovine serum albumin , epitope , antibody , immunology , molecular mimicry , antigen , biology , diabetes mellitus , medicine , endocrinology , fetal bovine serum , t cell , cell , immune system , biochemistry
Epidemiological and experimental evidence suggested that denial of dietary cow milk protein early in life protects genetically susceptible children and animals from insulin‐dependent diabetes (IDDM). Bovine serum albumin (BSA) was proposed as a candidate milk‐borne mimicry antigen responsible for the diabetogenic cow milk effect. Elevated anti‐BSA antibodies have been observed in patients and diabetic rodents, and these antibodies precipitate p69 from islet cell lysates. IDDM is a T ceil mediated disorder but efforts to detect BSA‐specific T cells in diabetic children have so far failed. We describe here a culture system which allowed the detection of BSA‐specific T cells and we mapped this response to the ABBOS peptide (pre‐BSA position 152–169) previously identified as a possible mimicry epitope. ABBOS sensitized T ceils were found in 28/31 children with recent onset TDDM but not in non‐diabetic controls nor in children with SLE or JRA. T cell proliferative responses declined within the first few years of diabetes diagnosis. Although no effector cell role for BSA/ABBOS specific T lymphocytes has been demonstrated, the presence of BSA peptide‐specific T cells strengthens the postulated link between a cow milk protein and IDDM.