A. Kipar et al., EXPRESSION OF MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II ANTIGEN IN NEOPLASTIC-CELLS OF CANINE CUTANEOUS HISTIOCYTOMA, Veterinary immunology and immunopathology, 62(1), 1998, pp. 1-13
Forty five cases of canine cutaneous histiocytoma (CCH) were examined
by immunohistology for expression and distribution of major histocompa
tibility complex (MHC) class II antigen in neoplastic cells. In additi
on, expression of lysozyme and calprotectin (leucocyte protein L1) in
neoplastic cells was investigated. Furthermore, B and T lymphocytes we
re demonstrated by antibodies against the CD3 antigen, IgG, and IgM. N
eoplastic cells showed two staining patterns for MHC class II antigen:
focal juxtanuclear cytoplasmic staining and/or rim-like staining alon
g the cell periphery. In 24 cases, a predominant or exclusive focal ju
xtanuclear cytoplasmic MHC class II antigen reaction in neoplastic cel
ls, and the presence of few diffusely distributed infiltrating CD3 ant
igen-positive T lymphocytes were observed. Tumors with numerous neopla
stic cells exhibiting staining for MHC class II antigen along the cell
periphery (n=21) showed increased inflammatory alterations, represent
ed by disseminated and nodular infiltrations of mainly CD3 antigen-pos
itive T cells. B cells, plasma cells, exudate macrophages, and neutrop
hils were rarely seen disseminated between neoplastic cells whereas th
eir number increased within focal inflammatory infiltrates, The focal
cytoplasmic reaction for MHC class II antigen in neoplastic cells migh
t represent newly synthesized MHC class Il molecules stored in vesicle
s, whereas staining of the cell periphery might occur due to accumulat
ion of MHC class II molecules along the plasma membrane. The increasin
g expression of MHC class II molecules on the cell surface might be th
e decisive factor for onset and progression of tumor regression. Howev
er, the exact mechanism of priming and activation of T cells by neopla
stic cells and the nature of the presented antigen are not yet known.
(C) 1998 Elsevier Science B.V.