Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immunity, Natural”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMedDate not supplied

[Adaptation of the immune system as a response to pregnancy].

INTRODUCTION: Pregnancy is an intriguing immunologic phenomenon. In spite of genetic differences, maternal and fetal cells are in close contact over the whole course of pregnancy with no evidence of either humoral and/or cellular immunologic response of mother to fetus as an allotransplant. The general opinion is that the fundamental protective mechanism must be located locally at the contact-plate, between the maternal and fetal tissues. Immunologic investigations proved the presence of specific systems which block the function of antipaternal maternal antibodies, as well as formation of cytotoxic maternal T-cells to paternal antigens. The system preventing rejection of graft during pregnancy is functioning at the level of maternal and fetal tissues. The protective mechanisms are coded by genes of MCH region, locus HLA-G. PROTECTIVE MECHANISMS IN THE PLACENTA: The placenta protects itself against antibody-mediated damage. A high level of complement-regulatory proteins (CD46, CD55 and CD59), being the response to the synthesis of complement-fixing maternal antibodies to paternal antigens and regulation of the placental HLA expression as a preventive reaction of the feto-placental unit to the influence of maternal CTL, are the most important protective mechanisms of placenta. PROTECTIVE MECHANISMS SHARED BY THE PLACENTA AND UTERUS: Protective mechanisms common both for placenta and uterus are as follows: expressions of Fas ligand prevention of infiltration of activated immune cells, regulation of immunosuppression which prevents proliferation of immune cells and high natural immunity (Na cells and macrophages) of the decidua.

Female↗
PubMed1976

Naturally acquired immunity to influenza type A: a clinical and laboratory study.

After type A influenza virus had undergone major antigenic change in mid 1968, it was noted that individuals previously infected by strains of the old subtype (Asian), especially late strains, appeared to be unexpectedly resistant to clinical attack by the new subtype (Hong Kong). Prospective studies have since shown that, during the A/England/42/72 influenza epidemic of 1972, in which the incidence was approximately 7% in the community, clinical influenza due to this virus was not found in 229 subjects previously confirmed as having had A/Hong Kong/1/68 influenza, even though vaccine which had been effective against A/Hong Kong/1/68 was ineffective against A/England/42/72. During the A/Port Chalmers/1/73 influenza epidemic of 1974, clinical influenza resulting from Port Chalmers virus was not found in a closely monitored group of 176 unvaccinated subjects previously infected by A/Hong Kong/1/68 or A/England/42/72, although laboratory studies demonstrated Port Chalmers infection in five of these (2-8%). By contrast, among 99 subjects who had no such history of earlier infection, 22 developed laboratory-proven Port Chalmers influenza and most of them had typical illness.

Adolescent↗
PubMed1977

Naturally acquired immunity to influenza type A: a further prospective study.

During the 1976 influenza epidemic, the incidence and severity of attack by A/Victoria/3/75 strain were studied in 312 participants who were divided into two groups: in Group 1 were 216 participants who had a history of laboratory-proven infection by one of the earlier strains of Hong Kong subtype; in Group 2 were 96 participants who had no known history of such prior infection. No participant in either group received influenza vaccine. The efficacy of clinical immunity, acquired as a result of prior infection by an earlier Hong Kong subtype strain, was judged by comparing the findings in Group 1 and Group 2. Incidence of laboratory-proven A/Victoria/3/75 infection was found to be 27% in Group 2 (26 cases confirmed) and 10.6% in Group 1 (23 cases confirmed). Among Group 1 members, the incidence was highest in those with the longest interval since prior Hong Kong subtype infection. Severe influenzal illness was seen in 14 of the 26 proven cases in Group 2, and in only three of the 23 proven cases in Group 1. The prior infection in these three had been by A/Hong Kong/1/68 strain in 1969-1970. Thus in Group 1, severe influenzal illness was not observed until six years or more had passed since prior infection (and three episodes of antigenic drift had intervened). Results suggested that low serum antibody levels may be unreliable as indicators of clinical immunity. Preepidemic sera of 99 members of Group 1 and 82 members of Group 2 showed no HAI antibody to A/Victoria/3/75 (titre less than 8), but the incidence of laboratory-proven A/Victoria/3/75 infection among these individuals was lower in Group 1 (19%) than in Group 2 (30.5%).

Adolescent↗
PubMed1985

Naturally acquired immunity to influenza type A. Lessons from two coexisting subtypes.

When the H1N1 subtype of influenza reappeared in the Northern Hemisphere during 1977, after a 20-year absence, it behaved very differently from the H3N2 subtype still in circulation. In Sydney, we studied the incidence of both subtypes of laboratory-proven influenza type A in 287 unvaccinated volunteers whose serum antibody titres were measured before and after each winter, to facilitate the detection of subclinical as well as clinical infection. During a 1977 epidemic, the A/Victoria/3/75 strain of the H3N2 subtype attacked participants of all age groups, whereas during epidemics of 1979 and 1981, the A/USSR/90/77 and A/Brazil/11/78 strains of the H1N1 subtype attacked only subjects born after 1950. The older participants apparently possessed homologous protection, acquired as a result of exposure to H1N1 more than 20 years earlier and not dependent upon strain-specific haemagglutination inhibition antibody.

Adolescent↗