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I read with interest the paper by Papadopoulos et al. describing the balance between type 1 and type 2 responses by CD4 and CD8 T lymphocytes in atopic asthmatics and normal subjects stimulated by rhinovirus. They state that their data is consistent with ‘reciprocal regulation of type 1 and type 2 responses’. Their figure demonstrates that in both normals and atopic asthmatics interferon gamma and in...
I read with interest the paper by Papadopoulos et al. describing the balance between type 1 and type 2 responses by CD4 and CD8 T lymphocytes in atopic asthmatics and normal subjects stimulated by rhinovirus. They state that their data is consistent with ‘reciprocal regulation of type 1 and type 2 responses’. Their figure demonstrates that in both normals and atopic asthmatics interferon gamma and interleukin 4 levels went up following rhinovirus stimulation relative to the normal controls. While I accept that there was a difference in the ratio between interferon gamma and interleukin 4 between the 2 groups of subjects, both groups had simultaneous rises in both type 1 and type 2 responses. These responses are not therefore reciprocal.
Type 1 and type 2 T helper cell responses have often been considered to be reciprocal. This has lead to the suggestion that the current high levels of allergic disease are a result of an adult type 2 dominated immune systems. This fails to take account of the fact that type 2 mediated diseases are associated with type 1 mediated diseases such as psoriasis, coeliac disease and type I diabetes in organs, in individuals and in populations.[2-5] There is also a parallel rise in the prevalence of type I diabetes and type 1 and type 2 mediated diseases share risk factors.[7-9] It therefore seems likely that while some factors may skew T cell development to either type 1 or type 2 some of the dominant influences may up regulate or down regulate both types of response.
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(2) Stene L, Magnus P, Lie R, Sovik O, Joner G, Group. tNCDS. Maternal and paternal age at delivery, birth order, and risk of childhood onset type I diabetes: population based cohort study. BMJ 2001;323:369-72.
(3) Simpson C, Anderson W, Helms P, Taylor M, Watson L, Prescott G, et al. Coincidence of immune-mediated diseases driven by Th1 and Th2 subsets suggests a common aetiology. Clin Exp Allergy 2002;2:37-42.
(4) Kero J, Gissler M, Hemminki E, Isolauri E. Could TH1 and TH2 diseases coexist? Evaluation of asthma incidence in children with coeliac disease type I diabetes, or rheumatoid arthritis: A register study. J Allergy Clin Immunol108(5):781-783.
(5) Olesen AB, Juul S, Birkebaek N, Thestrup-Pedersen K. Association between atopic dermatitis and insulin-dependent diabetes mellitus: a case-control study. Lancet 2001; 357:1749-52.
(6) Stene L, Nafstad P. Relation between the occurence of type I diabetes and asthma. Lancet 2001;357:607-8.
(7) Green A, Gale E, Patterson C. Incidence of childhood-onset insulin dependent diabetes mellitus: the EURODIAB ACE study. Lancet 1992;339:905-909.
(8) Gardner SG, Bingley PJ, Sawtell PA, Weeks S, Gale EA. Rising incidence of insulin dependent diabetes in children aged under 5 years in the Oxford region: time trend analysis. The Bart's-Oxford Study Group. BMJ 1997;315(7110):713-7.
(9) Patterson CC, Carson DJ, Hadden DR. Epidemiology of childhood IDDM in Northern Ireland 1989-1994: low incidence in areas with highest population density and most household crowding. Northern Ireland Diabetes Study Group. Diabetologia 1996;39(9):1063-9.