T-lymphocytic infiltration of the exocrine pancreas and liver in patie
nts with chronic pancreatitis has suggested that cell mediated immune
mechanisms may play a part in the pathogenesis of this disease. As exp
ression of major histocompatibility (MHC) antigens is a prerequisite f
or organ specific autoimmunity, the expression of HLA class I (beta2-m
icroglobulin) and class II (HLA-DR) determinants have been analysed, t
ogether with the presence of T-lymphocytes, in 93 patients (64 men and
29 women, mean age 40.6 years) having an operation for chronic pancre
atitis. Ethanol (63 patients), recurrent acute pancreatitis (12), cong
enital lesions (2), and unknown (16) were suggested to be the causes o
f the disease. Immunohistochemical staining of formalin fixed and para
ffin wax embedded tissue sections used conventional immunohistochemica
l techniques with specific anti-serum samples. No MHC expression was i
dentified in 10 histologically normal pancreatic control specimens or
in four cases of chronic pancreatitis secondary to obstruction by neur
oendocrine tumours within the head of the pancreas. Beta2-microglobuli
n expression by pancreatic exocrine epithelial cells was seen in 76 ch
ronic pancreatitis specimens (82%) while HLA-DR was present in 61 (66%
). Simultaneous expression of both class I and II determinants was see
n in 53 (57%) of cases. MHC determinant expression was not found in 10
cases (11%) of chronic pancreatitis. In the positive specimens, expre
ssion was confined to ductal and ductular (interlobular and intralobul
ar) epithelium with no staining of acinar cells. Staining was not rela
ted to the suspected cause of the disease or age. T-lymphocytes were m
ore prominent in chronic pancreatitis mean (SEM) (131 (15) cells per h
igh powered field) than controls (5 (1), p<0.01). Aberrant MHC express
ion by exocrine pancreatic ephithelial cells occurring in the presence
of an appreciable T-cell infiltration confirmed that the appropriate
cellular conditions were present for cell mediated cytotoxicity to con
tribute to the pathogenesis of chronic pancreatitis.