weak immune response studies, plenty more that show it if you want to find them:
http://www.ncbi.nlm.nih.gov/pubmed/16503465
Department of Medicine, University College London, London
BACKGROUND:
The cause of Crohn's disease has not been mechanistically proven. We tested the hypothesis that the disease is a form of immunodeficiency caused by impaired innate immunity.
METHODS:
We investigated inflammatory responses in patients and controls by quantifying neutrophil recruitment and cytokine production after acute trauma, interleukin 8 secretion by cultured monocyte-derived macrophages after exposure to inflammatory mediators, and local inflammatory and vascular changes in response to subcutaneous injection of heat-killed Escherichia coli.
FINDINGS:
In patients with Crohn's disease, trauma to rectum, ileum, or skin led to abnormally low neutrophil accumulation (differences from healthy individuals of 79%, n=8, p=0.0003; 57%, n=3, p=0.05; 50%, n=13, p<0.0001, respectively) and lower production of proinflammatory interleukin 8 (63%, n=7, p=0.003; 63%, n=3, p=0.05; 45%, n=8, p<0.0001) and interleukin 1beta (50%, n=8, p=0.0005). Interleukin 8 secretion by cultured macrophages was reduced after exposure to acute wound fluid (38%, n=50, p<0.0001), C5a (48%, n=41, p=0.0005), or tumour necrosis factor alpha (52%, n=27, p<0.0001). Local inflammatory reaction to inoculation with E coli was attenuated, as quantified by changes in bloodflow (ileal disease 50%, n=6, p=0.01; colonic disease 77%, n=6, p=0.0003). This response was mediated by nitric oxide in controls, was increased by sildenafil in patients, and was not related to CARD15 genotype.
INTERPRETATION:
In Crohn's disease,
a constitutionally weak immune response predisposes to accumulation of intestinal contents that breach the mucosal barrier of the bowel wall, resulting in granuloma formation and chronic inflammation. Polymorphisms in CARD15 do not underlie this phenotype, but incapacitate the NOD2 pathway that can compensate for impairment of innate inflammation. Current treatment of secondary chronic inflammation might exaggerate the underlying lesion and promote chronic disease.
http://gut.bmj.com/content/16/11/854.full.pdf
From the Division of Gastroenterology, Willhelmina Gasthuis and Binnengasthuis, University of Amsterdam,
The cellular immune system was studied in patients with Crohn's disease (CD), not receiving corticosteroids, or azathioprine, by means of in vitro and in vivo methods. It was found, that the in vitro lymphocyte reactivity of 54 CD patients after stimulation with a cocktail of antigens (varidase, trichophyton, candida, mumps, and PPD) was significantly depressed when compared with the response of 20 simultaneously cultured healthy controls (P < 0.001) or a group of 54 separately cultured healthy controls, matched for age and sex (P < 0.001). The lymphocyte response of a control group of 18 patients with malnutrition or malabsorption without any evidence of
inflammatory bowel disease, was higher than the response of an equal number of CD cases, although the difference failed to reach significance. Intradermally injection of the same five antigens, as used in the antigen cocktail, showed a
failure to react to any antigen in 13 out of 48 CD patients, in comparison with three out of 48 matched healthy controls (P < 0.01). In both CD patients, as well as in healthy controls a significant correlation could be demonstrated between the number of positive skin tests, the area of skin induration, and the in vitro lymphocyte responsiveness after stimulation with the antigen cocktail. In the CD group no correlation was found between in vitro responsiveness and disease activity, as defined by a score of clinical and biochemical parameters. The depressed skin reactivity and the hyporesponsiveness in the lymphocyte transformation test
after stimulation by an antigen cocktail suggest that
depression of the anamnestic cellular immune response is a basic feature in patients with Crohn's disease.
