<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lucas Sandri T</submitter><funding>BMBF (Bundesministerium für Bildung und Forschung)</funding><funding>EDCTP: European and Developing Countries Clinical Trials Partnership</funding><funding>CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico, Brasil)</funding><funding>CAPES (Coordenação de Aperfeiçoamento de Pessoal Superior)</funding><pagination>e0175973</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5435133</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(5)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Pathogens exert selective pressure which may lead to substantial changes in host immune responses. The human complement receptor type 1 (CR1) is an innate immune recognition glycoprotein that regulates the activation of the complement pathway and removes opsonized immune complexes. CR1 genetic variants in exon 29 have been associated with expression levels, C1q or C3b binding and increased susceptibility to several infectious diseases. Five distinct CR1 nucleotide substitutions determine the Knops blood group phenotypes, namely Kna/b, McCa/b, Sl1/Sl2, Sl4/Sl5 and KCAM+/-.&lt;h4>Methods&lt;/h4>CR1 variants were genotyped by direct sequencing in a cohort of 441 healthy individuals from Brazil, Vietnam, India, Republic of Congo and Ghana.&lt;h4>Results&lt;/h4>The distribution of the CR</pubmed_abstract><journal>PloS one</journal><pubmed_title>Geographical distribution of complement receptor type 1 variants and their associated disease risk.</pubmed_title><pmcid>PMC5435133</pmcid><funding_grant_id>BMBF BRA11/A33; 01DN11001</funding_grant_id><funding_grant_id>CANTAM (Central Africa Network on Tuberculosis, HIV/AIDs and Malaria)</funding_grant_id><pubmed_authors>Elumalai P</pubmed_authors><pubmed_authors>Valluri VL</pubmed_authors><pubmed_authors>Thangaraj K</pubmed_authors><pubmed_authors>Tong HV</pubmed_authors><pubmed_authors>Toan NL</pubmed_authors><pubmed_authors>Lucas Sandri T</pubmed_authors><pubmed_authors>Song LH</pubmed_authors><pubmed_authors>Adukpo S</pubmed_authors><pubmed_authors>Giang DP</pubmed_authors><pubmed_authors>Velavan TP</pubmed_authors><pubmed_authors>Ntoumi F</pubmed_authors><pubmed_authors>Nguetse CN</pubmed_authors><pubmed_authors>Jose de Messias Reason I</pubmed_authors><pubmed_authors>Kremsner PG</pubmed_authors><pubmed_authors>Meyer CG</pubmed_authors><pubmed_authors>Antunes Andrade F</pubmed_authors></additional><is_claimable>false</is_claimable><name>Geographical distribution of complement receptor type 1 variants and their associated disease risk.</name><description>&lt;h4>Background&lt;/h4>Pathogens exert selective pressure which may lead to substantial changes in host immune responses. The human complement receptor type 1 (CR1) is an innate immune recognition glycoprotein that regulates the activation of the complement pathway and removes opsonized immune complexes. CR1 genetic variants in exon 29 have been associated with expression levels, C1q or C3b binding and increased susceptibility to several infectious diseases. Five distinct CR1 nucleotide substitutions determine the Knops blood group phenotypes, namely Kna/b, McCa/b, Sl1/Sl2, Sl4/Sl5 and KCAM+/-.&lt;h4>Methods&lt;/h4>CR1 variants were genotyped by direct sequencing in a cohort of 441 healthy individuals from Brazil, Vietnam, India, Republic of Congo and Ghana.&lt;h4>Results&lt;/h4>The distribution of the CR</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017</publication><modification>2025-04-19T12:44:16.26Z</modification><creation>2019-03-26T22:53:05Z</creation></dates><accession>S-EPMC5435133</accession><cross_references><pubmed>28520715</pubmed><doi>10.1371/journal.pone.0175973</doi></cross_references></HashMap>