165
biotyping of the strains was according to the scheme of Lior.5,6 Of the 7 C laridis isolates, 5 were serotype 35, biotype I, and 2 were serotype 12, biotype I. The Cjejuni isolates belonged to serotype 36, biotype II, and serotype 41, biotype I, respectively. C. laridis was not isolated from 10 symptom-free persons. Their faecal specimens were also examined by electron microscopy for viruses and were
T-CELL SUBSET DISTRIBUTION IN MHC-CLASS 11 POSITIVE AND NEGATIVE COLORECTAL CARCINOMAS DETERMINED BY
QUANTITATIVE IMMUNOSTAINING
negative. The low isolation
rate
of C laridis and other
pathogens
can
probably be attributed to delays in specimen collection and because most specimens were not collected in transport medium. Unfortunately,
the
original samples of drinking
water were not
available for Campylobacter testing. Several weeks after the episode,
samples of the lake water collected in the vicinity of the station’s intake duct, frequented by large numbers of seagulls, yielded high faecal coliform counts. No campylobacters or salmonellae were detected in these samples with a membrane filtration technique followed by enrichment in selective media. Samples of seagull droppings were not available for analysis. Central Public Health Laboratory, Ontario Ministry of Health, Toronto
A. BROCZYK
Regional Public Health Laboratory, Peterborough, Ontario
S. THOMPSON D. SMITH
Enteric Bacteriology Division, Bureau of Microbiology, Laboratory Centre for Disease
Control, Ottawa, Ontario K1A 0L2, Canada
H. LIOR
1. Skirrow MB, Benjamin J. ’1001’ campylobacters: cultural characteristics of intestinal campylobacters from man and animals. J Hyg 1980; 85: 427-42. 2 Benjamin J, Leaper S, Owen RJ, Skirrow MB. Description of Campylobacter laridis, a new species comprising the nalidixic acid resistant thermophilic Campylobacter (NARTC) group. Curr Microbiol 1983; 8: 231-38. 3. Nachamkin I, Stowell C, Skalina D, Jones AM, Roop RM II, Smibert RM. Campylobacter laridis causing bacteremia in an immunosuppressed patient. Ann Intern Med 1984; 101: 55-57. 4. Tauxe RV, Patton CM, Edmonds P, Barrett TJ, Brenner DJ, Blake PA. Illness associated with Campylobacter laridis a newly recognized Campylobacter species. J Clin Microbiol 1985, 21: 222-25. 5. Lior H, Woodward DL, Edgar JA, Laroche LJ, Gill P. Serotyping of Campylobacter jejuni by slide agglutination based on heat-labile antigenic factors. J Clin Microbiol
1982; 15: 761-68. 6. Lior H. New extended biotyping scheme for Campylobacter jejuni, Campylobacter coli and "Campylobacter laridis". J Clin Microbiol 1984; 20: 636-40.
Results
as mean
(and SE) cells per high-power field.
respond to the physiological mediators which regulate class II expression on normal epithelia. This intrinsic inability, we suggest, properly exemplifies the "aberrant" state. The deficit could conceivably be at the level of the class II genes themselves or at the level of a transacting regulatory gene outside the major histocompatibility complex.6 Colorectal cancer cells in vitro do not invariably express class II antigens in response to y-interferon,7,811 HLA-D region products on macrophages, dendritic cells, vascular endothelial cells, and B cells are involved in the presentation of antigens to T cells.9 The demonstration of class II product-restricted antigen presentation by intestinal epithelium columnar cells in the rat10 is consistent with the hypothesis that intestinal epithelium participates directly in the regulation of gut mucosal immunity. Compromise of a comparable function on transformed human gut epithelial cells by complete or partial loss of class II molecules could prevent associative recognition by T helper/inducer cells of gut or putative tumour associated antigens. Department of Immunology, paterson Institute for Cancer Research, Christie Hospital and Holt Radium Institute, Manchester M20 9BX
MICHAEL MOORE ANNA K. GHOSH
1. Foulis AK. 2
Class II major histocompatibility complex and organ specific autoimmunity in man. J Pathol 1986; 150: 5-11. Selby WS, Janossy G, Mason DY, Jewell DP. Expression of HLA-DR antigens by colonic epithelium in inflammatory bowel disease. Clin Exp Immunol 1983; 53: 614-18
AS, Fabre JW. The membrane antigens of human colorectal cancer cells: Demonstration with monoclonal antibodies of heterogeneity within and between tumours and of anomalous expression of HLA-DR. Europ J Cancer Oncol 1983; 19: 209-20. 4. Momburg F, Degener T, Bacchus E, Moldenhauer G, Hammerling GJ, Moller P Loss of HLA-A,B,C, and de novo expression of HLA-D in colorectal cancer Int J Cancer 1986; 37: 179-84. 5. Ghosh AK, Moore M, Street AJ, Howat JMT, Schofield PF Expression of HLA-D sub-region products on human colorectal carcinoma. Int J Cancer 1986; 38: 459-64. 6. de Préval C, Lisowka-Grospierre B, Loche M, Griscelli C, Mach B. A trans-acting class II regulatory gene unlinked to the MHC controls expression of HLA class II genes. Nature 1985; 318: 291-93. 7. Pfizenmaier K, Bartson H, Scheurich P, et al. Differential &ggr;-interferon response of human colon carcinoma cells: Inhibition of proliferation and modulation of immunogenicity as independent effects of interferon on rumour cell growth. Cancer Res 1985; 45: 3503-09. 8. Moore M, Ghosh AK, Johnston D, Street AJ. Expression of MHC class II products on human colorectal cancer: an immunohistological and flow cytometnc study. J 3. Daar
"ABERRANT" MHC CLASS II EXPRESSION IN EPITHELIA
SiR—Dr Spencer and colleagues (Oct 25, p 983) suggest that the expression of class II antigens on epithelial tissues is a normal physiological event and that it is induced by lymphokine as generated by leucocytes in the microenvironment. Dr McNicol (Nov 29, pl282) finds class II antigens on the normal adrenal cortex in most samples and suggests that a mechanism other than lymphokine induction might be responsible for their expression, as in the epithelium of the lactating breast where the induction signal is hormonal. HLA-DR expression confined to residual pancreatic p cells in recent onset type I diabetes is unrelated to insulin, which also suggests that agents other than inflammatory mediators can induce class II antigens.’ Despite considerable variation within organs and between individuals, HLA-D antigen expression does seem to be a physiological property of most, if not all, normal epithelia. In the large intestine, class II antigens are rarely detectable on normal epithelial cells except in proximity to a pathological process. In chronic inflammatory bowel disease, the expression of HLA-DR antigens on inflamed epithelium is thought to result from a cell-mediated immune reaction within the mucosa, possibly directed against the epithelium.2 Class II antigens are also detectable
colorectal adenocarcinomas.3-5 In tumours, expression is frequently focal and may vary widely from 5 % to 90 % of the neoplastic population.5 However, in about one-third of colorectal cancers, class II antigens are undetectable, even though adjacent "normal" crypt epithelium may express class II antigens. Moreover, there is no apparent correlation between expression of antigens of the class II gene complex monitored by monoclonal antibody CR3/43 (anti-DP, -DQ, -DR monomorphic determinants) and lymphoid cell infiltration in this disease (table). These data indicate that a significant proportion of tumours fail to on
Immunogenet (in press). 9. Chestnut RW, Grey HM. Antigen presenting cells and mechanisms of antigen presentation. CRC Crit Rev Immunol 1985; 5: 263-316. 10. Bland PW, Warren LG. Antigen presentation by epithelial cells of the rat small intestine I: Kinetics, antigen specificity and blocking by Ia antisera. Immunology 1986; 58: 1-7.
TOSCANA VIRUS INFECTION IN UNITED STATES CITIZEN RETURNING FROM ITALY
SiR,—The May 25, 1985, issue of The Lancet contained reports of sandfly fever affecting Swedish troops in Cyprus1 and of neurovirulent Toscana virus (family Bunyaviridae, genus Phlebovirus) infection in a Swedish man who had visited Portugal.2 We too can report an infection with Toscana virus, acquired in another Mediterranean country, Italy. On July 6, 1985, a 66-year-old man was admitted to a Boston hospital complaining of mild frontal headache, myalgias, and fever (39’3°C) for a day and about 12 h of increasing confusion and inability to use words coherently. Physical examination revealed receptive and expressive dysphagia and mild neck stiffness. A low