The immunology of cellular stress proteins
Stress proteins or heat-shock proteins (HSP) are evolutionary conserved proteins present in every prokaryotic and eukaryotic cell. Their main function is to protect cells and proteins from damage under stressful circumstances. The latter circumstances do include the cell and protein damaging effects...
Saved in:
Superior document: | Frontiers Research Topics |
---|---|
: | |
Year of Publication: | 2014 |
Language: | English |
Series: | Frontiers Research Topics
|
Physical Description: | 1 electronic resource (89 p.) |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
id |
993548031404498 |
---|---|
ctrlnum |
(CKB)3710000000612081 (oapen)https://directory.doabooks.org/handle/20.500.12854/49989 (EXLCZ)993710000000612081 |
collection |
bib_alma |
record_format |
marc |
spelling |
Cristina Bonorino auth The immunology of cellular stress proteins Frontiers Media SA 2014 1 electronic resource (89 p.) text txt rdacontent computer c rdamedia online resource cr rdacarrier Frontiers Research Topics Stress proteins or heat-shock proteins (HSP) are evolutionary conserved proteins present in every prokaryotic and eukaryotic cell. Their main function is to protect cells and proteins from damage under stressful circumstances. The latter circumstances do include the cell and protein damaging effects of inflammation. The discovery of mycobacterial HSP60 being a critical antigen in the model of adjuvant arthritis, has led to studies that showed the immuno-dominance of microbial HSP60 and the potential of the microbial HSP induced repertoire of antibodies and T cells to cross-recognize the self-HSP homologues of stressed cells. Since then, the research in the immunology of stress proteins started to comprise a widening spectrum of topics with potential medical relevance. Interestingly, since stress proteins have their activities in both innate and adaptive immunity, they are key elements in the cross-roads between both arms of the immune system. Stress proteins or HSP can be considered as functional 'biomarkers' of inflammation. They are up-regulated locally during inflammation and interestingly, they seem to function as targets for anti-inflammatory regulatory T cells. In experimental models of autoimmunity, mainly arthritis, administration of HSP peptides have been shown to suppress disease. First clinical trials have shown the anti-inflammatory nature of T cell responses to Hsp. In type I diabetes and in rheumatoid arthritis, parenteral and oral administration of Hsp peptides were shown to induce a bias in pro-inflammatory T cells, switching them in the direction of regulatory cytokine production (IL4, IL5 and IL10). In addition a raised level of a marker of natural T regulatory cells, the transcription factor FoxP3, was noted in the RA trial. Other inflammatory diseases or diseases with inflammatory components which feature the immune imprint of the up-regulated Hsp are atherosclerosis, inflammatory bowel diseases, multiple sclerosis and atopic diseases such atopic dermatitis and allergic asthma. English Autoimmunity Heat shock proteins T cells T cell regulation Cancer 2-88919-325-X Willem Van Eden auth Ruurd Van Der Zee auth |
language |
English |
format |
eBook |
author |
Cristina Bonorino |
spellingShingle |
Cristina Bonorino The immunology of cellular stress proteins Frontiers Research Topics |
author_facet |
Cristina Bonorino Willem Van Eden Ruurd Van Der Zee |
author_variant |
c b cb |
author2 |
Willem Van Eden Ruurd Van Der Zee |
author2_variant |
w v e wve r v d z rvdz |
author_sort |
Cristina Bonorino |
title |
The immunology of cellular stress proteins |
title_full |
The immunology of cellular stress proteins |
title_fullStr |
The immunology of cellular stress proteins |
title_full_unstemmed |
The immunology of cellular stress proteins |
title_auth |
The immunology of cellular stress proteins |
title_new |
The immunology of cellular stress proteins |
title_sort |
the immunology of cellular stress proteins |
series |
Frontiers Research Topics |
series2 |
Frontiers Research Topics |
publisher |
Frontiers Media SA |
publishDate |
2014 |
physical |
1 electronic resource (89 p.) |
isbn |
2-88919-325-X |
illustrated |
Not Illustrated |
work_keys_str_mv |
AT cristinabonorino theimmunologyofcellularstressproteins AT willemvaneden theimmunologyofcellularstressproteins AT ruurdvanderzee theimmunologyofcellularstressproteins |
status_str |
n |
ids_txt_mv |
(CKB)3710000000612081 (oapen)https://directory.doabooks.org/handle/20.500.12854/49989 (EXLCZ)993710000000612081 |
carrierType_str_mv |
cr |
hierarchy_parent_title |
Frontiers Research Topics |
is_hierarchy_title |
The immunology of cellular stress proteins |
container_title |
Frontiers Research Topics |
author2_original_writing_str_mv |
noLinkedField noLinkedField |
_version_ |
1787548435047514112 |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>03035nam-a2200349z--4500</leader><controlfield tag="001">993548031404498</controlfield><controlfield tag="005">20231214133240.0</controlfield><controlfield tag="006">m o d </controlfield><controlfield tag="007">cr|mn|---annan</controlfield><controlfield tag="008">202102s2014 xx |||||o ||| 0|eng d</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(CKB)3710000000612081</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(oapen)https://directory.doabooks.org/handle/20.500.12854/49989</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(EXLCZ)993710000000612081</subfield></datafield><datafield tag="041" ind1="0" ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Cristina Bonorino</subfield><subfield code="4">auth</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">The immunology of cellular stress proteins</subfield></datafield><datafield tag="260" ind1=" " ind2=" "><subfield code="b">Frontiers Media SA</subfield><subfield code="c">2014</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">1 electronic resource (89 p.)</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">computer</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">online resource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="490" ind1="1" ind2=" "><subfield code="a">Frontiers Research Topics</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Stress proteins or heat-shock proteins (HSP) are evolutionary conserved proteins present in every prokaryotic and eukaryotic cell. Their main function is to protect cells and proteins from damage under stressful circumstances. The latter circumstances do include the cell and protein damaging effects of inflammation. The discovery of mycobacterial HSP60 being a critical antigen in the model of adjuvant arthritis, has led to studies that showed the immuno-dominance of microbial HSP60 and the potential of the microbial HSP induced repertoire of antibodies and T cells to cross-recognize the self-HSP homologues of stressed cells. Since then, the research in the immunology of stress proteins started to comprise a widening spectrum of topics with potential medical relevance. Interestingly, since stress proteins have their activities in both innate and adaptive immunity, they are key elements in the cross-roads between both arms of the immune system. Stress proteins or HSP can be considered as functional 'biomarkers' of inflammation. They are up-regulated locally during inflammation and interestingly, they seem to function as targets for anti-inflammatory regulatory T cells. In experimental models of autoimmunity, mainly arthritis, administration of HSP peptides have been shown to suppress disease. First clinical trials have shown the anti-inflammatory nature of T cell responses to Hsp. In type I diabetes and in rheumatoid arthritis, parenteral and oral administration of Hsp peptides were shown to induce a bias in pro-inflammatory T cells, switching them in the direction of regulatory cytokine production (IL4, IL5 and IL10). In addition a raised level of a marker of natural T regulatory cells, the transcription factor FoxP3, was noted in the RA trial. Other inflammatory diseases or diseases with inflammatory components which feature the immune imprint of the up-regulated Hsp are atherosclerosis, inflammatory bowel diseases, multiple sclerosis and atopic diseases such atopic dermatitis and allergic asthma.</subfield></datafield><datafield tag="546" ind1=" " ind2=" "><subfield code="a">English</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Autoimmunity</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Heat shock proteins</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">T cells</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">T cell regulation</subfield></datafield><datafield tag="653" ind1=" " ind2=" "><subfield code="a">Cancer</subfield></datafield><datafield tag="776" ind1=" " ind2=" "><subfield code="z">2-88919-325-X</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Willem Van Eden</subfield><subfield code="4">auth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ruurd Van Der Zee</subfield><subfield code="4">auth</subfield></datafield><datafield tag="906" ind1=" " ind2=" "><subfield code="a">BOOK</subfield></datafield><datafield tag="ADM" ind1=" " ind2=" "><subfield code="b">2023-12-15 05:47:47 Europe/Vienna</subfield><subfield code="f">system</subfield><subfield code="c">marc21</subfield><subfield code="a">2016-03-17 15:52:20 Europe/Vienna</subfield><subfield code="g">false</subfield></datafield><datafield tag="AVE" ind1=" " ind2=" "><subfield code="i">DOAB Directory of Open Access Books</subfield><subfield code="P">DOAB Directory of Open Access Books</subfield><subfield code="x">https://eu02.alma.exlibrisgroup.com/view/uresolver/43ACC_OEAW/openurl?u.ignore_date_coverage=true&portfolio_pid=5338751970004498&Force_direct=true</subfield><subfield code="Z">5338751970004498</subfield><subfield code="b">Available</subfield><subfield code="8">5338751970004498</subfield></datafield></record></collection> |