Association of MICA and NKG2D genetic variants with disease susceptibility and outcome of anti-TNF therapy in patients with axial spondyloarthritis
The disruption of the NKG2D-MICA axis can induce an enhanced immune response and promote autoimmune processes during axial spondyloarthritis (axSpA) pathogenesis. We aimed to investigate potential relationships between selected single nucleotide polymorphisms within the MICA and NKG2D genes and dise...
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| Veröffentlicht in: | Clinical and experimental rheumatology 2024-07, Vol.42 (7), p.1359 |
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| container_title | Clinical and experimental rheumatology |
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| creator | Wielińska, Joanna Bugaj, Bartosz Świerkot, Jerzy Kolossa, Katarzyna Iwaszko, Milena Jeka, Sławomir Bogunia-Kubik, Katarzyna |
| description | The disruption of the NKG2D-MICA axis can induce an enhanced immune response and promote autoimmune processes during axial spondyloarthritis (axSpA) pathogenesis. We aimed to investigate potential relationships between selected single nucleotide polymorphisms within the MICA and NKG2D genes and disease susceptibility and clinical parameters in axSpA patients treated with TNF inhibitors.
Genotyping of MICA rs1051792 and NKG2D rs1154831, rs1049174, and rs2255336 was performed in 163 axSpA patients and 234 healthy controls using a real-time PCR method.
MICA rs1051792 A allele was more common in patients than in controls (p |
| doi_str_mv | 10.55563/clinexprheumatol/l5346i |
| format | Article |
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Genotyping of MICA rs1051792 and NKG2D rs1154831, rs1049174, and rs2255336 was performed in 163 axSpA patients and 234 healthy controls using a real-time PCR method.
MICA rs1051792 A allele was more common in patients than in controls (p<0.0001). Patients with the AA genotype showed greater disease activity score (BASDAI) after three (p=4×10-4) and six (p=0.032) months of treatment compared to G carriers. After three months of therapy with anti-TNFs, the MICA AA homozygosity occurred more often in non-responsive or moderately responsive patients than good responders with the same genotype (p=1×10-4). Additionally, patients bearing the NKG2D rs1154831 CC genotype demonstrated lower BASDAI scores (p=0.035) and were significantly more common among subjects with a good outcome (p=0.004) after six months of treatment.
These results suggest that MICA and NKG2D gene polymorphisms may be biomarkers associated with disease susceptibility and clinical outcomes after anti-TNF therapy in axSpA patients and imply a rather less favourable effect of the MICA A and NKG2D G genetic variants.</description><identifier>ISSN: 0392-856X</identifier><identifier>ISSN: 1593-098X</identifier><identifier>EISSN: 1593-098X</identifier><identifier>DOI: 10.55563/clinexprheumatol/l5346i</identifier><identifier>PMID: 38372728</identifier><language>eng</language><publisher>Italy</publisher><subject>Adult ; Axial Spondyloarthritis - drug therapy ; Axial Spondyloarthritis - genetics ; Case-Control Studies ; Female ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; Histocompatibility Antigens Class I - genetics ; Humans ; Male ; Middle Aged ; NK Cell Lectin-Like Receptor Subfamily K - genetics ; Pharmacogenomic Variants ; Phenotype ; Polymorphism, Single Nucleotide ; Treatment Outcome ; Tumor Necrosis Factor Inhibitors - therapeutic use ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Clinical and experimental rheumatology, 2024-07, Vol.42 (7), p.1359</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38372728$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wielińska, Joanna</creatorcontrib><creatorcontrib>Bugaj, Bartosz</creatorcontrib><creatorcontrib>Świerkot, Jerzy</creatorcontrib><creatorcontrib>Kolossa, Katarzyna</creatorcontrib><creatorcontrib>Iwaszko, Milena</creatorcontrib><creatorcontrib>Jeka, Sławomir</creatorcontrib><creatorcontrib>Bogunia-Kubik, Katarzyna</creatorcontrib><title>Association of MICA and NKG2D genetic variants with disease susceptibility and outcome of anti-TNF therapy in patients with axial spondyloarthritis</title><title>Clinical and experimental rheumatology</title><addtitle>Clin Exp Rheumatol</addtitle><description>The disruption of the NKG2D-MICA axis can induce an enhanced immune response and promote autoimmune processes during axial spondyloarthritis (axSpA) pathogenesis. We aimed to investigate potential relationships between selected single nucleotide polymorphisms within the MICA and NKG2D genes and disease susceptibility and clinical parameters in axSpA patients treated with TNF inhibitors.
Genotyping of MICA rs1051792 and NKG2D rs1154831, rs1049174, and rs2255336 was performed in 163 axSpA patients and 234 healthy controls using a real-time PCR method.
MICA rs1051792 A allele was more common in patients than in controls (p<0.0001). Patients with the AA genotype showed greater disease activity score (BASDAI) after three (p=4×10-4) and six (p=0.032) months of treatment compared to G carriers. After three months of therapy with anti-TNFs, the MICA AA homozygosity occurred more often in non-responsive or moderately responsive patients than good responders with the same genotype (p=1×10-4). Additionally, patients bearing the NKG2D rs1154831 CC genotype demonstrated lower BASDAI scores (p=0.035) and were significantly more common among subjects with a good outcome (p=0.004) after six months of treatment.
These results suggest that MICA and NKG2D gene polymorphisms may be biomarkers associated with disease susceptibility and clinical outcomes after anti-TNF therapy in axSpA patients and imply a rather less favourable effect of the MICA A and NKG2D G genetic variants.</description><subject>Adult</subject><subject>Axial Spondyloarthritis - drug therapy</subject><subject>Axial Spondyloarthritis - genetics</subject><subject>Case-Control Studies</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>NK Cell Lectin-Like Receptor Subfamily K - genetics</subject><subject>Pharmacogenomic Variants</subject><subject>Phenotype</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Treatment Outcome</subject><subject>Tumor Necrosis Factor Inhibitors - therapeutic use</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0392-856X</issn><issn>1593-098X</issn><issn>1593-098X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkcFO3TAQRa2qVXlAfwF52U3AsWvHXiIoFBXoBiR2keNMeFM5cbAd4H1Hf7guj7JgMZrNuXfm6hJCa3YopVTiyHmc4HmOa1hGm4M_8lJ8U_iBrGppRMWMvvtIVkwYXmmp7nbIbkq_GeNKquYz2RFaNLzhekX-HKcUHNqMYaJhoFcXJ8fUTj29_nnOT-k9TJDR0Ucb0U450SfMa9pjApuApiU5mDN26DFvXmRhyS6M8M-q8FjdXJ_RvIZo5w3Fic7lELz52Ge0nqY5TP3GBxvzOmLGtE8-DdYn-PK698jt2febkx_V5a_z8t5l5WrDcmWUFmZQDnopZG9Y40A3uh60FrKDTnPGJZddiaoESCeaYTBKlemZltoZsUe-bn3nGB4WSLkdsQTy3k4QltRywwuoGNMF1VvUxZBShKGdI442btqatS-VtO8rabeVFOnB65WlG6F_E_7vQPwFptmQvQ</recordid><startdate>20240701</startdate><enddate>20240701</enddate><creator>Wielińska, Joanna</creator><creator>Bugaj, Bartosz</creator><creator>Świerkot, Jerzy</creator><creator>Kolossa, Katarzyna</creator><creator>Iwaszko, Milena</creator><creator>Jeka, Sławomir</creator><creator>Bogunia-Kubik, Katarzyna</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20240701</creationdate><title>Association of MICA and NKG2D genetic variants with disease susceptibility and outcome of anti-TNF therapy in patients with axial spondyloarthritis</title><author>Wielińska, Joanna ; Bugaj, Bartosz ; Świerkot, Jerzy ; Kolossa, Katarzyna ; Iwaszko, Milena ; Jeka, Sławomir ; Bogunia-Kubik, Katarzyna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c190t-96839f6ced535d907ce8781f8835beb8202525b83763e5c37ff966f96d0858c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adult</topic><topic>Axial Spondyloarthritis - drug therapy</topic><topic>Axial Spondyloarthritis - genetics</topic><topic>Case-Control Studies</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Histocompatibility Antigens Class I - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>NK Cell Lectin-Like Receptor Subfamily K - genetics</topic><topic>Pharmacogenomic Variants</topic><topic>Phenotype</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Treatment Outcome</topic><topic>Tumor Necrosis Factor Inhibitors - therapeutic use</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wielińska, Joanna</creatorcontrib><creatorcontrib>Bugaj, Bartosz</creatorcontrib><creatorcontrib>Świerkot, Jerzy</creatorcontrib><creatorcontrib>Kolossa, Katarzyna</creatorcontrib><creatorcontrib>Iwaszko, Milena</creatorcontrib><creatorcontrib>Jeka, Sławomir</creatorcontrib><creatorcontrib>Bogunia-Kubik, Katarzyna</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental rheumatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wielińska, Joanna</au><au>Bugaj, Bartosz</au><au>Świerkot, Jerzy</au><au>Kolossa, Katarzyna</au><au>Iwaszko, Milena</au><au>Jeka, Sławomir</au><au>Bogunia-Kubik, Katarzyna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of MICA and NKG2D genetic variants with disease susceptibility and outcome of anti-TNF therapy in patients with axial spondyloarthritis</atitle><jtitle>Clinical and experimental rheumatology</jtitle><addtitle>Clin Exp Rheumatol</addtitle><date>2024-07-01</date><risdate>2024</risdate><volume>42</volume><issue>7</issue><spage>1359</spage><pages>1359-</pages><issn>0392-856X</issn><issn>1593-098X</issn><eissn>1593-098X</eissn><abstract>The disruption of the NKG2D-MICA axis can induce an enhanced immune response and promote autoimmune processes during axial spondyloarthritis (axSpA) pathogenesis. We aimed to investigate potential relationships between selected single nucleotide polymorphisms within the MICA and NKG2D genes and disease susceptibility and clinical parameters in axSpA patients treated with TNF inhibitors.
Genotyping of MICA rs1051792 and NKG2D rs1154831, rs1049174, and rs2255336 was performed in 163 axSpA patients and 234 healthy controls using a real-time PCR method.
MICA rs1051792 A allele was more common in patients than in controls (p<0.0001). Patients with the AA genotype showed greater disease activity score (BASDAI) after three (p=4×10-4) and six (p=0.032) months of treatment compared to G carriers. After three months of therapy with anti-TNFs, the MICA AA homozygosity occurred more often in non-responsive or moderately responsive patients than good responders with the same genotype (p=1×10-4). Additionally, patients bearing the NKG2D rs1154831 CC genotype demonstrated lower BASDAI scores (p=0.035) and were significantly more common among subjects with a good outcome (p=0.004) after six months of treatment.
These results suggest that MICA and NKG2D gene polymorphisms may be biomarkers associated with disease susceptibility and clinical outcomes after anti-TNF therapy in axSpA patients and imply a rather less favourable effect of the MICA A and NKG2D G genetic variants.</abstract><cop>Italy</cop><pmid>38372728</pmid><doi>10.55563/clinexprheumatol/l5346i</doi></addata></record> |
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| subjects | Adult Axial Spondyloarthritis - drug therapy Axial Spondyloarthritis - genetics Case-Control Studies Female Gene Frequency Genetic Association Studies Genetic Predisposition to Disease Histocompatibility Antigens Class I - genetics Humans Male Middle Aged NK Cell Lectin-Like Receptor Subfamily K - genetics Pharmacogenomic Variants Phenotype Polymorphism, Single Nucleotide Treatment Outcome Tumor Necrosis Factor Inhibitors - therapeutic use Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - genetics |
| title | Association of MICA and NKG2D genetic variants with disease susceptibility and outcome of anti-TNF therapy in patients with axial spondyloarthritis |
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