The Age-Dependent Role of Th22, Tc22, and Tc17 Cells in the Severity of Pneumonia in COVID-19 Immunopathogenesis
Coronavirus disease 2019 (COVID-19) has clinical manifestations ranging from mild symptoms to respiratory failure, septic shock, and multi-organ failure. Lymphocytes are divided into different subtypes based on their cytokine production pattern. In this study, we investigated the role of cytokine ex...
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| Veröffentlicht in: | Viral immunology 2022-05, Vol.35 (4), p.318-327 |
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| creator | Cagan, Eren Tezcan, Gulcin Simsek, Abdurrahman Kizmaz, Muhammed Ali Dombaz, Fatma Asan, Ali Demir, H Ibrahim Bal, Haldun Yoyen Ermis, Digdem Gorek Dilektasli, Aslı Kazak, Esra Akalin, E Halis Oral, H Barbaros Budak, Ferah |
| description | Coronavirus disease 2019 (COVID-19) has clinical manifestations ranging from mild symptoms to respiratory failure, septic shock, and multi-organ failure. Lymphocytes are divided into different subtypes based on their cytokine production pattern. In this study, we investigated the role of cytokine expressions of CD4
+
T (T helper [Th]1, Th2, Th17, Th22) and CD8
+
T cell subtypes (T cytotoxic [Tc]1, Tc2, Tc17, Tc22) in the pathogenesis of COVID-19. Peripheral blood mononuclear cells (PBMCs) were extracted with Ficoll by density gradient centrifugation from blood samples of 180 COVID-19 patients (children and adults) and 30 healthy controls. PBMCs were stimulated with PMA and Ionomycin and treated with Brefeldin A in the fourth hour, and a 10-colored monoclonal antibody panel was evaluated at the end of the sixth hour using flow cytometry. According to our findings, the numbers of Th22 (CD3
+
, CD4
+
, and interleukin [IL]-22
+
) and Tc22 (CD3
+
, CD8
+
, IL-22
+
) cells increased in adult patients regardless of the level of pneumonia (mild, severe, or symptom-free) as compared with healthy controls (
p
|
| doi_str_mv | 10.1089/vim.2021.0132 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2646717732</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2646717732</sourcerecordid><originalsourceid>FETCH-LOGICAL-c365t-73ca90599f588680b1db0535c89abb57c4553c021816e22b450faa42e6b9627c3</originalsourceid><addsrcrecordid>eNqFkUtLxDAUhYMoOj6WbiXgxoUd82geXcqMjwFB0dFtSTO3TqVNatMK_ntTRl24cXNzuflyODcHoWNKppTo7OKjaqaMMDollLMtNKFCqERnSm6jCdGaJZqlYg_th_BGCNFS8120xwWXnGg6Qe1yDfjyFZI5tOBW4Hr86GvAvsTLNWPneGnHatwqdlThGdR1wJXDfXz3BB_QVf3nSD84GBrvKjNezu5fFvOEZnjRNIPzrenX_hUchCocop3S1AGOvs8D9Hx9tZzdJnf3N4vZ5V1iuRR9org1GRFZVgodTZOCrgoiuLA6M0UhlE2F4DburakExopUkNKYlIEsMsmU5QfobKPbdv59gNDnTRVsdG8c-CHkTKZSUaU4i-jpH_TND52L7iIlBU2V1Gmkkg1lOx9CB2XedlVjus-cknyMIo9R5GMU-RhF5E--VYeigdUv_fP3EeAbYBwb5-oKCuj6f2S_AKPEkS0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2665147684</pqid></control><display><type>article</type><title>The Age-Dependent Role of Th22, Tc22, and Tc17 Cells in the Severity of Pneumonia in COVID-19 Immunopathogenesis</title><source>Alma/SFX Local Collection</source><creator>Cagan, Eren ; Tezcan, Gulcin ; Simsek, Abdurrahman ; Kizmaz, Muhammed Ali ; Dombaz, Fatma ; Asan, Ali ; Demir, H Ibrahim ; Bal, Haldun ; Yoyen Ermis, Digdem ; Gorek Dilektasli, Aslı ; Kazak, Esra ; Akalin, E Halis ; Oral, H Barbaros ; Budak, Ferah</creator><creatorcontrib>Cagan, Eren ; Tezcan, Gulcin ; Simsek, Abdurrahman ; Kizmaz, Muhammed Ali ; Dombaz, Fatma ; Asan, Ali ; Demir, H Ibrahim ; Bal, Haldun ; Yoyen Ermis, Digdem ; Gorek Dilektasli, Aslı ; Kazak, Esra ; Akalin, E Halis ; Oral, H Barbaros ; Budak, Ferah</creatorcontrib><description>Coronavirus disease 2019 (COVID-19) has clinical manifestations ranging from mild symptoms to respiratory failure, septic shock, and multi-organ failure. Lymphocytes are divided into different subtypes based on their cytokine production pattern. In this study, we investigated the role of cytokine expressions of CD4
+
T (T helper [Th]1, Th2, Th17, Th22) and CD8
+
T cell subtypes (T cytotoxic [Tc]1, Tc2, Tc17, Tc22) in the pathogenesis of COVID-19. Peripheral blood mononuclear cells (PBMCs) were extracted with Ficoll by density gradient centrifugation from blood samples of 180 COVID-19 patients (children and adults) and 30 healthy controls. PBMCs were stimulated with PMA and Ionomycin and treated with Brefeldin A in the fourth hour, and a 10-colored monoclonal antibody panel was evaluated at the end of the sixth hour using flow cytometry. According to our findings, the numbers of Th22 (CD3
+
, CD4
+
, and interleukin [IL]-22
+
) and Tc22 (CD3
+
, CD8
+
, IL-22
+
) cells increased in adult patients regardless of the level of pneumonia (mild, severe, or symptom-free) as compared with healthy controls (
p
< 0.05). In addition, the number of Tc17 (CD3
+
, CD8
+
, and IL-17A
+
) cells increased in low pneumonia and severe pneumonia groups compared with the healthy controls (
p
< 0.05). Both IL-22 and IL-17A production decreased during a follow-up within 6 weeks of discharge. Our findings suggest that the increase in only IL-22 expressed Tc22 cells in the 0–12 age group with a general symptom-free course and higher levels of Th22 and Tc22 in uncomplicated adult cases may indicate the protective effect of IL-22. On the contrary, the association between the severity of pneumonia and the elevation of Tc17 cells in adults may reveal the damaging effect of IL-22 when it is co-expressed with IL-17.</description><identifier>ISSN: 0882-8245</identifier><identifier>EISSN: 1557-8976</identifier><identifier>DOI: 10.1089/vim.2021.0132</identifier><identifier>PMID: 35363081</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc., publishers</publisher><subject>Adults ; Brefeldin A ; CD3 antigen ; CD4 antigen ; CD8 antigen ; Centrifugation ; Coronaviruses ; COVID-19 ; Cytokines ; Cytotoxicity ; Flow cytometry ; Helper cells ; Immunopathogenesis ; Interleukin 17 ; Interleukin 22 ; Ionomycin ; Leukocytes (mononuclear) ; Lymphocytes T ; Monoclonal antibodies ; Original Articles ; Patients ; Peripheral blood mononuclear cells ; Pneumonia ; Respiratory failure ; Septic shock</subject><ispartof>Viral immunology, 2022-05, Vol.35 (4), p.318-327</ispartof><rights>2022, Mary Ann Liebert, Inc., publishers</rights><rights>Copyright Mary Ann Liebert, Inc. May 2022</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-73ca90599f588680b1db0535c89abb57c4553c021816e22b450faa42e6b9627c3</citedby><cites>FETCH-LOGICAL-c365t-73ca90599f588680b1db0535c89abb57c4553c021816e22b450faa42e6b9627c3</cites><orcidid>0000-0001-5871-8769 ; 0000-0001-7625-9148</orcidid></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/35363081$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cagan, Eren</creatorcontrib><creatorcontrib>Tezcan, Gulcin</creatorcontrib><creatorcontrib>Simsek, Abdurrahman</creatorcontrib><creatorcontrib>Kizmaz, Muhammed Ali</creatorcontrib><creatorcontrib>Dombaz, Fatma</creatorcontrib><creatorcontrib>Asan, Ali</creatorcontrib><creatorcontrib>Demir, H Ibrahim</creatorcontrib><creatorcontrib>Bal, Haldun</creatorcontrib><creatorcontrib>Yoyen Ermis, Digdem</creatorcontrib><creatorcontrib>Gorek Dilektasli, Aslı</creatorcontrib><creatorcontrib>Kazak, Esra</creatorcontrib><creatorcontrib>Akalin, E Halis</creatorcontrib><creatorcontrib>Oral, H Barbaros</creatorcontrib><creatorcontrib>Budak, Ferah</creatorcontrib><title>The Age-Dependent Role of Th22, Tc22, and Tc17 Cells in the Severity of Pneumonia in COVID-19 Immunopathogenesis</title><title>Viral immunology</title><addtitle>Viral Immunol</addtitle><description>Coronavirus disease 2019 (COVID-19) has clinical manifestations ranging from mild symptoms to respiratory failure, septic shock, and multi-organ failure. Lymphocytes are divided into different subtypes based on their cytokine production pattern. In this study, we investigated the role of cytokine expressions of CD4
+
T (T helper [Th]1, Th2, Th17, Th22) and CD8
+
T cell subtypes (T cytotoxic [Tc]1, Tc2, Tc17, Tc22) in the pathogenesis of COVID-19. Peripheral blood mononuclear cells (PBMCs) were extracted with Ficoll by density gradient centrifugation from blood samples of 180 COVID-19 patients (children and adults) and 30 healthy controls. PBMCs were stimulated with PMA and Ionomycin and treated with Brefeldin A in the fourth hour, and a 10-colored monoclonal antibody panel was evaluated at the end of the sixth hour using flow cytometry. According to our findings, the numbers of Th22 (CD3
+
, CD4
+
, and interleukin [IL]-22
+
) and Tc22 (CD3
+
, CD8
+
, IL-22
+
) cells increased in adult patients regardless of the level of pneumonia (mild, severe, or symptom-free) as compared with healthy controls (
p
< 0.05). In addition, the number of Tc17 (CD3
+
, CD8
+
, and IL-17A
+
) cells increased in low pneumonia and severe pneumonia groups compared with the healthy controls (
p
< 0.05). Both IL-22 and IL-17A production decreased during a follow-up within 6 weeks of discharge. Our findings suggest that the increase in only IL-22 expressed Tc22 cells in the 0–12 age group with a general symptom-free course and higher levels of Th22 and Tc22 in uncomplicated adult cases may indicate the protective effect of IL-22. On the contrary, the association between the severity of pneumonia and the elevation of Tc17 cells in adults may reveal the damaging effect of IL-22 when it is co-expressed with IL-17.</description><subject>Adults</subject><subject>Brefeldin A</subject><subject>CD3 antigen</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>Centrifugation</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Flow cytometry</subject><subject>Helper cells</subject><subject>Immunopathogenesis</subject><subject>Interleukin 17</subject><subject>Interleukin 22</subject><subject>Ionomycin</subject><subject>Leukocytes (mononuclear)</subject><subject>Lymphocytes T</subject><subject>Monoclonal antibodies</subject><subject>Original Articles</subject><subject>Patients</subject><subject>Peripheral blood mononuclear cells</subject><subject>Pneumonia</subject><subject>Respiratory failure</subject><subject>Septic shock</subject><issn>0882-8245</issn><issn>1557-8976</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNqFkUtLxDAUhYMoOj6WbiXgxoUd82geXcqMjwFB0dFtSTO3TqVNatMK_ntTRl24cXNzuflyODcHoWNKppTo7OKjaqaMMDollLMtNKFCqERnSm6jCdGaJZqlYg_th_BGCNFS8120xwWXnGg6Qe1yDfjyFZI5tOBW4Hr86GvAvsTLNWPneGnHatwqdlThGdR1wJXDfXz3BB_QVf3nSD84GBrvKjNezu5fFvOEZnjRNIPzrenX_hUchCocop3S1AGOvs8D9Hx9tZzdJnf3N4vZ5V1iuRR9org1GRFZVgodTZOCrgoiuLA6M0UhlE2F4DburakExopUkNKYlIEsMsmU5QfobKPbdv59gNDnTRVsdG8c-CHkTKZSUaU4i-jpH_TND52L7iIlBU2V1Gmkkg1lOx9CB2XedlVjus-cknyMIo9R5GMU-RhF5E--VYeigdUv_fP3EeAbYBwb5-oKCuj6f2S_AKPEkS0</recordid><startdate>20220501</startdate><enddate>20220501</enddate><creator>Cagan, Eren</creator><creator>Tezcan, Gulcin</creator><creator>Simsek, Abdurrahman</creator><creator>Kizmaz, Muhammed Ali</creator><creator>Dombaz, Fatma</creator><creator>Asan, Ali</creator><creator>Demir, H Ibrahim</creator><creator>Bal, Haldun</creator><creator>Yoyen Ermis, Digdem</creator><creator>Gorek Dilektasli, Aslı</creator><creator>Kazak, Esra</creator><creator>Akalin, E Halis</creator><creator>Oral, H Barbaros</creator><creator>Budak, Ferah</creator><general>Mary Ann Liebert, Inc., publishers</general><general>Mary Ann Liebert, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5871-8769</orcidid><orcidid>https://orcid.org/0000-0001-7625-9148</orcidid></search><sort><creationdate>20220501</creationdate><title>The Age-Dependent Role of Th22, Tc22, and Tc17 Cells in the Severity of Pneumonia in COVID-19 Immunopathogenesis</title><author>Cagan, Eren ; Tezcan, Gulcin ; Simsek, Abdurrahman ; Kizmaz, Muhammed Ali ; Dombaz, Fatma ; Asan, Ali ; Demir, H Ibrahim ; Bal, Haldun ; Yoyen Ermis, Digdem ; Gorek Dilektasli, Aslı ; Kazak, Esra ; Akalin, E Halis ; Oral, H Barbaros ; Budak, Ferah</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-73ca90599f588680b1db0535c89abb57c4553c021816e22b450faa42e6b9627c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adults</topic><topic>Brefeldin A</topic><topic>CD3 antigen</topic><topic>CD4 antigen</topic><topic>CD8 antigen</topic><topic>Centrifugation</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Flow cytometry</topic><topic>Helper cells</topic><topic>Immunopathogenesis</topic><topic>Interleukin 17</topic><topic>Interleukin 22</topic><topic>Ionomycin</topic><topic>Leukocytes (mononuclear)</topic><topic>Lymphocytes T</topic><topic>Monoclonal antibodies</topic><topic>Original Articles</topic><topic>Patients</topic><topic>Peripheral blood mononuclear cells</topic><topic>Pneumonia</topic><topic>Respiratory failure</topic><topic>Septic shock</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cagan, Eren</creatorcontrib><creatorcontrib>Tezcan, Gulcin</creatorcontrib><creatorcontrib>Simsek, Abdurrahman</creatorcontrib><creatorcontrib>Kizmaz, Muhammed Ali</creatorcontrib><creatorcontrib>Dombaz, Fatma</creatorcontrib><creatorcontrib>Asan, Ali</creatorcontrib><creatorcontrib>Demir, H Ibrahim</creatorcontrib><creatorcontrib>Bal, Haldun</creatorcontrib><creatorcontrib>Yoyen Ermis, Digdem</creatorcontrib><creatorcontrib>Gorek Dilektasli, Aslı</creatorcontrib><creatorcontrib>Kazak, Esra</creatorcontrib><creatorcontrib>Akalin, E Halis</creatorcontrib><creatorcontrib>Oral, H Barbaros</creatorcontrib><creatorcontrib>Budak, Ferah</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Viral immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cagan, Eren</au><au>Tezcan, Gulcin</au><au>Simsek, Abdurrahman</au><au>Kizmaz, Muhammed Ali</au><au>Dombaz, Fatma</au><au>Asan, Ali</au><au>Demir, H Ibrahim</au><au>Bal, Haldun</au><au>Yoyen Ermis, Digdem</au><au>Gorek Dilektasli, Aslı</au><au>Kazak, Esra</au><au>Akalin, E Halis</au><au>Oral, H Barbaros</au><au>Budak, Ferah</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Age-Dependent Role of Th22, Tc22, and Tc17 Cells in the Severity of Pneumonia in COVID-19 Immunopathogenesis</atitle><jtitle>Viral immunology</jtitle><addtitle>Viral Immunol</addtitle><date>2022-05-01</date><risdate>2022</risdate><volume>35</volume><issue>4</issue><spage>318</spage><epage>327</epage><pages>318-327</pages><issn>0882-8245</issn><eissn>1557-8976</eissn><abstract>Coronavirus disease 2019 (COVID-19) has clinical manifestations ranging from mild symptoms to respiratory failure, septic shock, and multi-organ failure. Lymphocytes are divided into different subtypes based on their cytokine production pattern. In this study, we investigated the role of cytokine expressions of CD4
+
T (T helper [Th]1, Th2, Th17, Th22) and CD8
+
T cell subtypes (T cytotoxic [Tc]1, Tc2, Tc17, Tc22) in the pathogenesis of COVID-19. Peripheral blood mononuclear cells (PBMCs) were extracted with Ficoll by density gradient centrifugation from blood samples of 180 COVID-19 patients (children and adults) and 30 healthy controls. PBMCs were stimulated with PMA and Ionomycin and treated with Brefeldin A in the fourth hour, and a 10-colored monoclonal antibody panel was evaluated at the end of the sixth hour using flow cytometry. According to our findings, the numbers of Th22 (CD3
+
, CD4
+
, and interleukin [IL]-22
+
) and Tc22 (CD3
+
, CD8
+
, IL-22
+
) cells increased in adult patients regardless of the level of pneumonia (mild, severe, or symptom-free) as compared with healthy controls (
p
< 0.05). In addition, the number of Tc17 (CD3
+
, CD8
+
, and IL-17A
+
) cells increased in low pneumonia and severe pneumonia groups compared with the healthy controls (
p
< 0.05). Both IL-22 and IL-17A production decreased during a follow-up within 6 weeks of discharge. Our findings suggest that the increase in only IL-22 expressed Tc22 cells in the 0–12 age group with a general symptom-free course and higher levels of Th22 and Tc22 in uncomplicated adult cases may indicate the protective effect of IL-22. On the contrary, the association between the severity of pneumonia and the elevation of Tc17 cells in adults may reveal the damaging effect of IL-22 when it is co-expressed with IL-17.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc., publishers</pub><pmid>35363081</pmid><doi>10.1089/vim.2021.0132</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5871-8769</orcidid><orcidid>https://orcid.org/0000-0001-7625-9148</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0882-8245 |
| ispartof | Viral immunology, 2022-05, Vol.35 (4), p.318-327 |
| issn | 0882-8245 1557-8976 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2646717732 |
| source | Alma/SFX Local Collection |
| subjects | Adults Brefeldin A CD3 antigen CD4 antigen CD8 antigen Centrifugation Coronaviruses COVID-19 Cytokines Cytotoxicity Flow cytometry Helper cells Immunopathogenesis Interleukin 17 Interleukin 22 Ionomycin Leukocytes (mononuclear) Lymphocytes T Monoclonal antibodies Original Articles Patients Peripheral blood mononuclear cells Pneumonia Respiratory failure Septic shock |
| title | The Age-Dependent Role of Th22, Tc22, and Tc17 Cells in the Severity of Pneumonia in COVID-19 Immunopathogenesis |
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