PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Complement C7”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 289 records · Page 16Linked to original sources
PubMed1978

Inherited deficiency of the sixth component of complement: a silent or null gene.

Four families have been studied, some members of which have inherited deficiency of the sixth component of complement. The genetically determined electrophoretic variants of C6 were evaluated in all family members. Seven individuals were found who did not have the variant found in the serum of the parent from whom they inherited the deficiency. It is inferred that the isolated low levels of C6 in these individuals results from the heterozygous state of a normal C6 variant gene and a silent or null C6 gene; the genes determining electrophoretic variants and the low serum levels of C6 are allelic.

Alleles↗
PubMed1983

Leukocyte complement: a possible role for C5 in lymphocyte stimulation.

The results presented here show that Fab' antibody fragments directed to complement proteins C5, C6, and C7 inhibit lymphocyte stimulation in mixed lymphocyte culture (MLC) by up to 65%, as determined by decreased incorporation of 3H-thymidine. Lymphocyte stimulation induced by PHA-mitogen was also inhibited up to 100% by anti-C5 Fab'. Specificity of these reactions was established by the findings that goat anti-C5 or murine hybridoma anti-C5 both inhibited MLC; the inhibitory activity of anti-C5 Fab' was absorbed with highly purified C5 (but not with C3), and antibody directed to C3 did not inhibit lymphocyte stimulation by MLC or PHA. The effects of anti-C5 were exerted in a nontoxic manner. Cleavage of lymphocyte associated C5 with factor B (Bb) or with trypsin resulted in stimulation of lymphocyte thymidine incorporation. Purified C5a was found to induce lymphocyte stimulation in serum-free medium in pulse-chase types of experiments. Anti-C6 and C7 Fab' also inhibited lymphocyte stimulation induced in one-way MLC. These results suggest that C5, C5a, and/or C6 and C7 may play a role in triggering of lymphocyte blastogenesis.

Animals↗
PubMed1978

The complement profile in relation to the "reactor" state: a study in the immediate post-partum period.

C56 (activated "reactor") could be generated by adding zymosan to only nineteen out of the fifty serum samples obtained from southern Chinese women 3 to 5 days after a normal spontaneous delivery. As a group, post-partum sera showed a 25% increase in total haemolytic complement, an almost two-fold increase in haemolytic C5, C4 and C8 plus C9 activity, a 50% increase in antigenic C3 and haemolytic C2, C1 and factor B activity, a less than 20% increase in haemolytic C6 and C7 activity, and a 20% decrease in factor D and C1 inhibitor activity. Consequently, their C5:C7 ratios were significantly elevated. This finding supports, in part, the theory that the "reactor" state or ability to generate C56 depends on a relative excess of C56 over C7. However, comparison of the complement profile between sera with and those without "reactor" activity did not reveal any difference, except a greater elevation of C5 in the latter. It appears possible that a grossly excessive level of C5 may, in fact, be unfavourable to the generation of C56.

Complement C5↗
PubMed1975

A case of deficiency of the seventh component of complement in man. Biological properties of a C7-deficient serum and description of a C7-inactivating principle.

The serum of a 13-year-old healthy boy was found to be deficient in whole complement activity. The seventh component of complement could not be detected by functional assays whereas the titres of the other components were found within the normal range. An attempt to detect C7 by immunodiffusion against an antiserum to human C7 also failed. The functions of C1-C6 were normal with respect to opsonizing activity, immune adherence, and the ability to generate chemotactic activity. However, those functions that require the whole complement sequence such as bactericidal and haemolytic activity were found to be absent. Furthermore, the occurrence of a C7-inactivating principle was demonstrated in the C7-deficient serum. This principle inactivated C7 both in the fluid phase and in its cell-bound state. Some physicochemical parameters of the inactivator are described and its possible nature is discussed.

Adolescent↗
PubMed1987

Hereditary complement deficiency in survivors of meningococcal disease: high prevalence of C7/C8 deficiency in Sephardic (Moroccan) Jews.

The prevalence of complement deficiency was studied among 111 survivors of sporadic meningococcal disease located through the medical records of 10 Israeli hospitals. There were 11 patients with CH50 = 0: one with systemic lupus erythematosus and 10 with hereditary terminal complement deficiency (four with homozygous C7 and six with C8 deficiency). There was no hereditary complement deficiency among 39 Ashkenazi subjects as against 18 per cent among 38 Sephardi subjects and 40 per cent among 15 of Moroccan ancestry (p less than 0.05). The age at first presentation of meningococcal disease in complement deficient patients was 14.7 +/- 7.6, years compared with 8.1 +/- 10.9 in the non-deficient patients (p less than 0.025). None of the complement deficient patients had meningitis below the age of 5 years vs. 49 per cent of non-deficient subjects. Recurrent meningitis was observed in 40 vs. 4 per cent (p less than 0.01) and meningitis in siblings in 40 vs. 2 per cent respectively (p less than 0.001). In addition to the 10 propositi, 11 non-propositus siblings were identified with severe complement deficiency (six with homozygous C7 and five with C8 deficiency). Seven of the non-propositi had no history at all of meningitis or any other serious systemic disease, underlining the relatively favourable prognosis of terminal complement deficiency. With increasing familiarity with the clinical features of this hereditary disease, it is possible now to identify on clinical grounds patients with meningococcal disease with a high likelihood of terminal complement deficiency.

Adolescent↗