| 1. |
- Albin, B, et al.
(författare)
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Mortality among 723 948 foreign- and native-born Swedes 1970-1999
- 2005
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Ingår i: European Journal of Public Health. - Oxford, UK : Oxford University Press (OUP). - 1101-1262 .- 1464-360X. ; 15:5, s. 511-517
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Tidskriftsartikel (refereegranskat)abstract
- Background: Mortality in a population is regarded as an accurate and valid measure of the population's health. There are a few international studies, predominantly cross- sectional, of mortality among all foreign- born compared with an indigenous population, and the results have varied. No Swedish longitudinal study describing and analysing mortality data was found in a literature review. Methods: This study describes and analyses the differences in mortality between foreign- born persons and native Swedes during the period 1970 - 1999, based on data from Statistics Sweden and the National Board of Health and Welfare. The database consisted of 723 948 persons, 361 974 foreign- born living in Sweden in 1970, aged >= 16 years, and 361 974 Swedish controls matched for age, sex, occupation and type of employment, living in the same county in 1970. Results: The results showed increased mortality for foreign- born persons compared with the Swedish controls [ odds ratio ( OR) 1.08; 95% confidence interval ( CI) 1.07 - 1.08]. Persons who had migrated ` late' ( 1941 - 1970) to Sweden were 2.5 years younger at time of death than controls. In relation to country of birth, the highest risk odds were for men born in Finland ( OR 1.21), Denmark ( OR 1.11) and Norway/ Iceland ( OR 1.074). Age cohorts of foreign- born persons born between 1901 and 1920 had higher mortality at age 55 - 69 years than cohorts born between 1921 and 1944. Conclusions: Migrants had higher mortality than the native population, and migration may be a risk factor for health; therefore, this seems to be an important factor to consider when studying mortality and health.
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| 2. |
- Hjelm, F, et al.
(författare)
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Antibody-mediated regulation of the immune response
- 2006
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 64:3, s. 177-184
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Tidskriftsartikel (refereegranskat)abstract
- Antibodies administered in vivo together with the antigen they are specific for can regulate the immune response to that antigen. This phenomenon is called antibody-mediated feedback regulation and has been known for over 100 years. Both passively administered and actively produced antibodies exert immunoregulatory functions. Feedback regulation can be either positive or negative, resulting in >1000-fold enhancement or >99% suppression of the specific antibody response. Usually, the response to the entire antigen is up- or downregulated, regardless of which epitope the regulating antibody recognizes. IgG of all isotypes can suppress responses to large particulate antigens like erythrocytes, a phenomenon used clinically in Rhesus prophylaxis. IgG suppression works in mice lacking the known Fc-gamma receptors (FcgammaR) and a likely mechanism of action is epitope masking. IgG1, IgG2a and IgG2b administered together with soluble protein antigens will enhance antibody and CD4+ T-cell responses via activating FcgammaR, probably via increased antigen presentation by dendritic cells. IgG3 as well as IgM also enhance antibody responses but their effects are dependent on their ability to activate complement. A possible mechanism is increased B-cell activation caused by immune complexes co-crosslinking the B-cell receptor with the complement-receptor 2/CD19 receptor complex, known to lower the threshold for B-cell activation. IgE-antibodies enhance antibody and CD4+ T-cell responses to small soluble proteins. This effect is entirely dependent on the low-affinity receptor for IgE, CD23, the mechanism probably being increased antigen presentation by CD23+ B cells.
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| 3. |
- Hjelm, F, et al.
(författare)
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IgG3-mediated enhancement of the antibody response is normal in Fc gammaRI-deficient mice
- 2005
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 62:5, s. 453-461
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Tidskriftsartikel (refereegranskat)abstract
- Antibodies, administered together with their specific antigen, can feedback-regulate antibody responses to this antigen. IgG1, IgG2a and IgG2b enhance antibody responses to soluble protein antigens. This effect is primarily mediated by FcRs as enhancement is impaired in FcR gamma-/- mice, reported to lack Fc gammaRI and Fc gammaRIII because of deletion of the common FcR gamma chain. Also IgG3 can enhance antibody responses. However, this effect is unperturbed in FcR gamma-/- mice but severely impaired in complement-depleted animals and in animals lacking complement receptor 1 and 2. Although this argues against involvement of Fc gammaRs, FcR gamma-/- mice may express one-fifth of the normal levels of Fc gammaRI and, in addition, Fc gammaRI has been suggested to bind IgG3. We re-investigated the dependence of IgG3-mediated enhancement on Fc gammaRs using a mouse strain selectively lacking Fc gammaRI and found that IgG3-mediated enhancement is completely normal. Unlike IgE and IgG2a, which are both thought to enhance T-cell proliferation via FcR-mediated antigen presentation, IgG3 was a poor enhancer of T-cell proliferation both in vivo and in vitro. These findings argue against a significant involvement of Fc gammaRs in IgG3-mediated enhancement of antibody responses and support our previous conclusion that complement plays a major role.
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