lukaszaw

Scavenius C, Nikolajsen CL, Stenvang M, Thogersen IB, Wyrozemski L, Wisniewski HG, Otzen DE, Sanggaard KW, Enghild JJ (2016). The compact and biologically relevant structure of inter-α-inhibitor is maintained by the chondroitin sulfate chain and divalent cations. J Biol Chem. 291(9):4658-70. doi: 10.1074/jbc.M115.678748.

• Clarke, Alexander W.; Bozek, Lilla; Babalola, Abayomi I.; Wyrozemski, Lukasz; Paynter, Vanessa Molin & Vinther, Jakob [Show all 15 contributors for this article] (2026). Genomic contingence beneath ecological convergence: the tempo and mode of gene loss in parasitic bilaterians. Evolution. ISSN 0014-3820. 80(9), p. 2062–2081. doi: 10.1093/evolut/qpag126. Full text in Research Archive Show summary

  Parasitism has independently evolved hundreds of times among metazoans. Nonetheless, parasites have explored only a limited range of ecologies, and they display frequent convergence in morphological, behavioral, and life-history traits. Although gene loss in particular parasitic species has been documented, it is not known if gene loss converges along the same lines as these other traits. To test for convergent gene loss, we characterized the housekeeping, regulatory, and DNA-repair complements of 48 bilaterian species, including 20 parasites belonging to 6 different bilaterian phyla. We found that different parasitic strategies do not display characteristic tempos or modes of gene loss. Further, the accelerated rates of gene loss seen in some parasites were almost always shared with their free-living relatives, indicating that the increased rate of loss preceded the rise of parasitism. Therefore, the convergent ecological strategies and adaptations that have arisen in distantly related parasitic lineages overlay contingent gene losses, which largely reflect their phylogenetic history. These results have important implications for how ecologists and evolutionary biologists should model the acquisition of parasitism, especially regarding the long-held assumption that reversion from a parasitic to a free-living state is impossible.

• Clarke, Alexander W.; Høye, Eirik; Hembrom, Anju Angelina; Paynter, Vanessa Molin; Vinther, Jakob & Wyrozemski, Lukasz [Show all 22 contributors for this article] (2025). MirGeneDB 3.0: Improved taxonomic sampling, uniform nomenclature of novel conserved microRNA families and updated covariance models. Nucleic Acids Research (NAR). ISSN 0305-1048. 53(D1), p. D116–D128. doi: 10.1093/nar/gkae1094. Full text in Research Archive
• Yao, Ying; Wyrozemski, Lukasz Adam; Lundin, Knut; Sandve, Geir Kjetil Ferkingstad & Qiao, Shuo Wang (2021). Differential expression profile of gluten-specific T cells identified by single-cell RNA-seq. PLOS ONE. 16:e0258029(10), p. 1–17. doi: 10.1371/journal.pone.0258029. Full text in Research Archive Show summary

  Gluten-specific CD4 + T cells drive the pathogenesis of celiac disease and circulating gluten-specific T cells can be identified by staining with HLA-DQ:gluten tetramers. In this first single-cell RNA-seq study of tetramer-sorted T cells from untreated celiac disease patients blood, we found that gluten-specific T cells showed distinct transcriptomic profiles consistent with activated effector memory T cells that shared features with Th1 and follicular helper T cells. Compared to non-specific cells, gluten-specific T cells showed differential expression of several genes involved in T-cell receptor signaling, translational processes, apoptosis, fatty acid transport, and redox potentials. Many of the gluten-specific T cells studied shared T-cell receptor with each other, indicating that circulating gluten-specific T cells belong to a limited number of clones. Moreover, the transcriptional profiles of cells that shared the same clonal origin were transcriptionally more similar compared with between clonally unrelated gluten-specific cells.

• Wyrozemski, Lukasz Adam & Qiao, Shuo Wang (2021). Immunobiology and conflicting roles of the human CD161 receptor in T cells. Scandinavian Journal of Immunology. ISSN 0300-9475. 94:e13090(3), p. 1–8. doi: 10.1111/sji.13090. Full text in Research Archive Show summary

  Human C-type lectin-like CD161 is a type-II transmembrane protein expressed on the surface of various lymphocytes across innate and adaptive immune systems. CD161+ T cells displayed enhanced ability to produce cytokines and were shown to be enriched in the gut. Independently of function, CD161 was used as marker of innate-like T cells and marker of IL-17-producing cells. The function of CD161 is still not fully understood. In T cells, CD161 was proposed to act as co-signalling receptor that influence T-cell receptor-dependent responses. However, conflicting studies were published demonstrating lack of agreement over the role of CD161 during T-cell activation. In this review, we outline phenotypical and functional consequences of CD161 expression in T cells. We provide critical discussion over the most pressing issues including in depth evaluation of the literature concerning CD161 putative co-signalling properties.

• Wyrozemski, Lukasz Adam; Sollid, Ludvig Magne & Qiao, Shuo Wang (2020). C-type lectin-like CD161 is not a co-signalling receptor in gluten-reactive CD4 + T cells. Scandinavian Journal of Immunology. ISSN 0300-9475. 00:e13016, p. 1–9. doi: 10.1111/sji.13016. Full text in Research Archive Show summary

  C‐type lectin‐like CD161, a class II transmembrane protein, is a surface receptor expressed by NK cells and T cells. In coeliac disease, CD161 was expressed more frequently on gluten‐reactive CD4 + T cells compared to other memory CD4 + T cells isolated from the same tissue compartment. CD161 is a putative co‐signalling molecule that was proposed to act as co‐stimulatory receptor in the context of signalling through TCR, but contradicting results were published. In order to understand the role of CD161 in gluten‐reactive CD4 + T cells, we combined T cell stimulation assays or T cell proliferation assays with ligation of CD161 and intracellular cytokine staining. We found that CD161 ligation provided neither co‐stimulatory nor co‐inhibitory signals to modulate proliferation and IFN‐γ or IL‐21 production by gluten‐reactive CD4 + T cell clones. Thus, we suggest that CD161 does not function as a co‐signalling receptor in the context of gluten‐reactive CD4 + T cells.

• Sikkeland, Liv Ingunn Bjoner; Qiao, Shuo Wang; Ueland, Thor; Myrdal, Ole Henrik; Wyrozemski, Lukasz Adam & Aukrust, Pål [Show all 12 contributors for this article] (2020). Lung CD4+ T cells in patients with lung fibrosis produce pro-fibrotic IL-13 together with IFNγ. European Respiratory Journal. ISSN 0903-1936. 57:2000983(3), p. 1–4. doi: 10.1183/13993003.00983-2020. Full text in Research Archive Show summary

  Progressive fibrosing interstitial lung diseases (PF-ILD) have poor prognosis and survival, and their pathogenesis is not well understood[1]. Mechanistically, lung fibrosis is thought to result from distorted wound-healing following tissue insults and inflammation, leading to scar formation by excess deposition of extracellular matrix proteins and destruction of lung architecture[2]. The fibrotic process is complex, and CD4+ T cells are likely involved by their production of a wide range of cytokines and growth factors that promote fibroblast proliferation and differentiation, collagen production, and stimulate production of pro-fibrotic mediators by tissue macrophages[3]. However, CD4+ T cells in PF-ILD are poorly characterized. To this end, we performed a detailed analysis of phenotype, cytokine production and clonality of T cells from the lungs [bronchoalveolar lavage (BAL)] of PF-ILD patients. We found that BAL from PF-ILD lungs contained high numbers of clonally expanded CD4+ T cells that produced an unusual combination of interferon (IFN)  and pro-fibrotic interleukin (IL)-13. Such cells were not found in patient blood or in control BAL samples.

• Yao, Ying; Zia, Asima; Wyrozemski, Lukasz Adam; Lindeman, Ida; Sandve, Geir Kjetil & Qiao, Shuo Wang (2018). Exploiting antigen receptor information to quantify index switching in single-cell transcriptome sequencing experiments. PLOS ONE. 13(12), p. 1–17. doi: 10.1371/journal.pone.0208484. Full text in Research Archive Show summary

  By offering high sequencing speed and ultra-high-throughput at a low price, Illumina next-generation sequencing platforms have been widely adopted in recent years. However, an experiment with multiplexed library could be at risk of molecular recombination, known as “index switching”, which causes a proportion of the reads to be assigned to an incorrect sample. It is reported that a new advance, exclusion amplification (ExAmp) in conjunction with the patterned flow cell technology introduced on HiSeq 3000/HiSeq 4000/HiSeq X sequencing systems, potentially suffers from a higher rate of index switching than conventional bridge amplification. We took advantage of the diverse but highly cell-specific expression of antigen receptors on immune cells to quantify index switching on single cell RNA-seq data that were sequenced on HiSeq 3000 and HiSeq 4000. By utilizing the unique antigen receptor expression, we could quantify the spread-of-signal from many different wells (n = 55 from total of three batches) due to index switching. Based on full-length T cell receptor (TCR) sequences from all samples reconstructed by TraCeR and TCR gene expression quantified by Kallisto, we found index switching in all three batches of experiments investigated. The median percentage of incorrectly detected markers was estimated to be 3.9% (interquartile range (IQR): 1.7%-7.3%). We did not detect any consistent patterns of certain indices to be more prone to switching than others, suggesting that index switching is a stochastic process. Our results confirm that index switching is a problem that affects samples run in multiplexed libraries on Illumina HiSeq 3000 and HiSeq 4000 platforms.

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