Trynka Group | Immune Genomics

Trynka Group | Immune Genomics

Trynka Group


Our Research and Approach

A large proportion of human DNA sequences are identical when individual people are compared. However, each of us also carries many differences in DNA sequence (genetic variants). The vast majority of these variants are harmless, e.g. they can contribute to the normal variability in individuals; however, some variants have been linked to diseases. A plethora of genetic variants are currently linked to common diseases that affect the immune system, such as type 1 diabetes, rheumatoid arthritis, celiac disease and inflammatory bowel disease amongst others.

The molecular mechanisms by which genetic variants predispose an individual to the development of immune diseases are largely unknown. Many of these variants localise close to DNA sequences which do not code for proteins (genes), indicating that they may have a gene regulatory function in immune cells. We do not however, understand the exact mechanisms through which these variants may act to disrupt critical molecular pathways that cause diseases. Our group combines immunologic and genomic assays to study the human immune system with a goal to map genetic variants to functional cellular effects.

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Dr Gosia Trynka
Group Leader

Gosia leads the immune genomics group who study how human genetic variation impacts immune system and predisposes to development of autoimmune diseases.

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Programmes, Associate Research Programmes and Facilities

Partners and Funders

Internal Partners


  • Partitioning heritability by functional annotation using genome-wide association summary statistics.

    Finucane HK, Bulik-Sullivan B, Gusev A, Trynka G, Reshef Y et al.

    Nature genetics 2015;47;11;1228-35

  • Disentangling the Effects of Colocalizing Genomic Annotations to Functionally Prioritize Non-coding Variants within Complex-Trait Loci.

    Trynka G, Westra HJ, Slowikowski K, Hu X, Xu H et al.

    American journal of human genetics 2015;97;1;139-52

  • Partitioning heritability of regulatory and cell-type-specific variants across 11 common diseases.

    Gusev A, Lee SH, Trynka G, Finucane H, Vilhjálmsson BJ et al.

    American journal of human genetics 2014;95;5;535-52

  • Regulation of gene expression in autoimmune disease loci and the genetic basis of proliferation in CD4+ effector memory T cells.

    Hu X, Kim H, Raj T, Brennan PJ, Trynka G et al.

    PLoS genetics 2014;10;6;e1004404

  • Genetics of rheumatoid arthritis contributes to biology and drug discovery.

    Okada Y, Wu D, Trynka G, Raj T, Terao C et al.

    Nature 2014;506;7488;376-81

  • Using chromatin marks to interpret and localize genetic associations to complex human traits and diseases.

    Trynka G and Raychaudhuri S

    Current opinion in genetics & development 2013;23;6;635-41

  • Chromatin marks identify critical cell types for fine mapping complex trait variants.

    Trynka G, Sandor C, Han B, Xu H, Stranger BE et al.

    Nature genetics 2013;45;2;124-30

  • Bayesian inference analyses of the polygenic architecture of rheumatoid arthritis.

    Stahl EA, Wegmann D, Trynka G, Gutierrez-Achury J, Do R et al.

    Nature genetics 2012;44;5;483-9

  • Dense genotyping identifies and localizes multiple common and rare variant association signals in celiac disease.

    Trynka G, Hunt KA, Bockett NA, Romanos J, Mistry V et al.

    Nature genetics 2011;43;12;1193-201

  • Meta-analysis of genome-wide association studies in celiac disease and rheumatoid arthritis identifies fourteen non-HLA shared loci.

    Zhernakova A, Stahl EA, Trynka G, Raychaudhuri S, Festen EA et al.

    PLoS genetics 2011;7;2;e1002004

  • Multiple common variants for celiac disease influencing immune gene expression.

    Dubois PC, Trynka G, Franke L, Hunt KA, Romanos J et al.

    Nature genetics 2010;42;4;295-302

  • Common and different genetic background for rheumatoid arthritis and coeliac disease.

    Coenen MJ, Trynka G, Heskamp S, Franke B, van Diemen CC et al.

    Human molecular genetics 2009;18;21;4195-203

  • Coeliac disease-associated risk variants in TNFAIP3 and REL implicate altered NF-kappaB signalling.

    Trynka G, Zhernakova A, Romanos J, Franke L, Hunt KA et al.

    Gut 2009;58;8;1078-83

  • Detection, imputation, and association analysis of small deletions and null alleles on oligonucleotide arrays.

    Franke L, de Kovel CG, Aulchenko YS, Trynka G, Zhernakova A et al.

    American journal of human genetics 2008;82;6;1316-33

  • Genetic analysis of innate immunity in Crohn's disease and ulcerative colitis identifies two susceptibility loci harboring CARD9 and IL18RAP.

    Zhernakova A, Festen EM, Franke L, Trynka G, van Diemen CC et al.

    American journal of human genetics 2008;82;5;1202-10

  • Newly identified genetic risk variants for celiac disease related to the immune response.

    Hunt KA, Zhernakova A, Turner G, Heap GA, Franke L et al.

    Nature genetics 2008;40;4;395-402

  • Immunochip meta-analysis in European and Argentinian populations identifies two novel genetic loci associated with celiac disease.

    Ricaño-Ponce I, Gutierrez-Achury J, Costa AF, Deelen P, Kurilshikov A et al.

    European journal of human genetics : EJHG 2019

  • Chromatin activity at GWAS loci identifies T cell states driving complex immune diseases.

    Soskic B, Cano-Gamez E, Smyth DJ, Rowan WC, Nakic N et al.

    Nature genetics 2019;51;10;1486-1493

  • Gene expression variability across cells and species shapes innate immunity.

    Hagai T, Chen X, Miragaia RJ, Rostom R, Gomes T et al.

    Nature 2018;563;7730;197-202

  • Beating the odds to secure a permanent contract.

    Smaglik P

    Nature 2018;562;7725;S49-S51

  • Coloc-stats: a unified web interface to perform colocalization analysis of genomic features.

    Simovski B, Kanduri C, Gundersen S, Titov D, Domanska D et al.

    Nucleic acids research 2018