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N G Papadopoulos, L A Stanciu, A Papi, S T Holgate, S L Johnston
A defective type 1 response to rhinovirus in atopic asthma
Thorax 2002; 57: 328-332 [Abstract][Full text][PDF]

Electronic letters published:

[Read eLetter]Are type 1 and type 2 reponses really reciprocal?
Wendy JA Anderson   (22 May 2002)

Are type 1 and type 2 reponses really reciprocal? 22 May 2002
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Wendy JA Anderson,
Concultant Respiratory Physician
United Hospitals NHS trust.

Send letter to journal:
Re: Are type 1 and type 2 reponses really reciprocal?

wendy.anderson{at}uh.n-i.nhs.uk Wendy JA Anderson

Dear Editor

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.[1] 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.

References

(1) Holt PG, Macaubas PA, Stumbles PA, Sly PD. The role of allergy in the development of asthma. Nature 1999;402(Supp):B12-17.

(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.

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