Publication:
Transfusion-related immunomodulation

dc.contributor.buuauthorBal, Salih Haldun
dc.contributor.buuauthorBAL, SALİH HALDUN
dc.contributor.buuauthorOral, Haluk Barbaros
dc.contributor.buuauthorORAL, HALUK BARBAROS
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentİmmünoloji Ana Bilim Dalı
dc.contributor.orcid0000-0003-0463-6818
dc.contributor.researcheridHJY-9001-2023
dc.contributor.researcheridK-7285-2012
dc.date.accessioned2024-09-30T12:05:04Z
dc.date.available2024-09-30T12:05:04Z
dc.date.issued2016-12-01
dc.description.abstractAlthough allogeneic blood transfusion (ABT) is a valuable medical practice, it has some critical complications. One of these complications is transfusion-related immunomodulation (TRIM). Transfusion-related immunomodulation describes the changes and its results in recipient's immune system after ABT. After ABT, some outcomes may be observed in the recipient including increased graft survival, decreased Crohn's disease recurrences and recurrent spontaneous abortuses, increased postoperative bacterial infections, cancer recurrences and mortality, and reactivation of latent infections such as cytomegalovirus and human immunodeficiency virus. It has been postulated that TRIM may originate from leukocytes within the product, biologic response modifiers-immunologic mediators (BRM-IM) that accumulate within the plasma or soluble human leukocyte antigen-class I molecules within the allogeneic plasma. Also, some properties of erythrocytes, storage time of blood components, and the number of transfused products are accused of TRIM development. However, main factors held responsible for TRIM development are allogeneic leukocytes and related BRM-IMs. It is thought that mechanisms such as clonal deletion, immunosuppression, anergy, microchimerism, the polarization of the immune response from T helper 1 (Th1) to Th2 and, apoptosis in the recipient immune system may cause TRIM. For this reason, leukoreduction is suggested for prevention. However, this application may not be efficient since reasons other than leukocytes may limit leukoreduction.
dc.identifier.doi10.5606/tji.2016.525
dc.identifier.endpage46
dc.identifier.issn1301-109X
dc.identifier.issue3
dc.identifier.startpage37
dc.identifier.urihttps://doi.org/10.5606/tji.2016.525
dc.identifier.urihttps://hdl.handle.net/11452/45519
dc.identifier.volume4
dc.identifier.wos000395319800002
dc.indexed.wosWOS.ESCI
dc.language.isoen
dc.publisherTurkish Soc Immunology
dc.relation.journalTurkish Journal Of Immunology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectRed-blood-cells
dc.subjectRegulatory t-cells
dc.subjectRandomized controlled-trial
dc.subjectIndependent risk-factor
dc.subjectAcute lung injury
dc.subjectPeripheral-blood
dc.subjectPostoperative infection
dc.subjectCancer recurrence
dc.subjectCardiac-surgery
dc.subjectFas ligand
dc.subjectImmunomodulation
dc.subjectLeukoreduction
dc.subjectTransfusion
dc.subjectTransfusion-related immunomodulation
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectImmunology
dc.titleTransfusion-related immunomodulation
dc.typeReview
dspace.entity.typePublication
local.contributor.departmentTıp Fakültesi/Dr Raşit Durusoy Kan Merkezi
local.contributor.departmentTıp Fakültesi/İmmünoloji Ana Bilim Dalı
relation.isAuthorOfPublicationa539e15c-3358-43ad-a410-a601c8d8760d
relation.isAuthorOfPublicationbc853dab-a811-42b9-b03b-6d5fe067efe8
relation.isAuthorOfPublication.latestForDiscoverya539e15c-3358-43ad-a410-a601c8d8760d

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