Immunologic changes after transfusion of autologous or allogeneic buffy coat‐poor versus WBC‐reduced blood transfusions in patients undergoing arthroplasty.II. Activation of T cells, macrophages, and cell‐mediated lympholysis

Innerhofer, Petra; Tilz, Gernot P.; Fuchs, Dietmar; Luz, G.; Hobisch-Hagen, Petra; Schobersberger, Wolfgang; Nußbaumer, Walter; Lochs, A.; Irschick, Eveline U.

doi:10.1046/j.1537-2995.2000.40070821.x

Cited by 36 publications

(23 citation statements)

References 25 publications

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“…aBt is thought to bear the risk to induce a status of relative immunosuppression in the host by a decrease of natural killer cell activity, phagocytic activity, an increase in suppressor t-cell activity with inhibition of interleukin 2, and sfas ligand and shla molecule transfusion. [22][23][24][25][26][27] it has been hypothesized that disseminated tumor cells in patients undergoing potentially curative resections might escape immunologic surveillance and thereby disseminate predisposing the individual to an earlier recurrence. 22 transfusion-acquired immunomodulation after oncologic resection has been attributed as a potential risk factor for earlier recurrence best described for colorectal and hepatocellular carcinomas, as well as carcinoma of the pancreas.…”

Section: Discussionmentioning

confidence: 99%

Impact of Perioperative Allogeneic Red Blood Cell Transfusion on Recurrence and Overall Survival After Resection of Colorectal Liver Metastases

Schiergens

Rentsch

Kasparek

et al. 2015

Diseases of the Colon &Amp; Rectum

109

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Section: Discussionmentioning

confidence: 99%

Impact of Perioperative Allogeneic Red Blood Cell Transfusion on Recurrence and Overall Survival After Resection of Colorectal Liver Metastases

Schiergens

Rentsch

Kasparek

et al. 2015

Diseases of the Colon &Amp; Rectum

109

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“…At the same time, T-cell numbers and function remain suppressed for up to 3 weeks after injury [21,34,35]. However, elevations of sIL-2R and neopterin, representing a sustained activation of the IFN-γ and TNF pathways, are not necessarily synonymous for an efficient immune response [36]. Although our data indicate a negative correlation between serum T 3 and sIL-2R, similarly to the findings by Boelen et al [5], we disagree with their conclusion implicating the low T 3 syndrome as the consequence rather than the cause of activation of the cytokine network.…”

Section: Discussionmentioning

confidence: 99%

Low T3 Syndrome in Head-Injured Patients is Associated with Prolonged Suppression of Markers of Cell-Mediated Immune Response

et al. 2005

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European Journal of Trauma Ab stractPurpose: To clarify the association between disturbed thyroid hormone metabolism (low T 3 syndrome) and release of cytokines and markers of cell-mediated immune response. Material and Methods: Concentrations of cytokines as well as of thyroid hormones were determined in 32 patients suffering from severe traumatic brain injury: interleukin-(IL-)1, IL-6, IL-10, tumor necrosis factor, transforming growth factor-(TGF-)β, soluble interleukin-2 receptor (sIL-2R), neopterin, and β 2 -microglobulin (β2m) in serum and cerebrospinal fluid; triiodothyronine (T 3 ), free T 3 , thyroxine (T 4 ), free T 4 , thyrotropin, thyroxine-binding globulin, and albumin in serum. Additionally, clinical parameters were assessed: Glasgow Coma Score, CT scan, intracranial pressure, Glasgow Outcome Score, and occurrence of pneumonia. Results: Among 31 patients with a low T 3 syndrome, those with additional low serum T 4 levels (n = 13) showed a prolonged suppression of serum β2m, neopterin, and sIL-2R, and a higher secondary increase of serum β2m, neopterin, and TGF-β, as well as lower T 3 levels (all p < 0.05). These patients also had a longer stay in the intensive care unit (34 ± 6 days vs. 22 ± 12 days; p = 0.008). Increased levels of β2m correlated with a preceding decrease of thyrotropin (cerebrospinal fluid: r = -0.53; p = 0.004; serum: r = -0.41; p = 0.029). Associations of thyroid hormone metabolism with either other cytokines or with clinical parameters were not detected. Conclusion:These results show that low T3 syndrome is a very common pathophysiological feature after severe traumatic brain injury. The association of a low T 3 syndrome in combination with low serum T 4 levels, with an altered time course of markers of cell-mediated immunity led the authors to hypothesize that a disturbed thyroid hormone metabolism may be interrelated with a prolonged cellular immune dysfunction after traumatic brain injury.

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“…The combination of suppressed T-cell proliferation (mixed lymphocyte culture test; MLC test), diminished cytolytic effector reaction (cell-mediated lymphocytotoxicity; CML) with continuous release of sIL-2R, s-TNFr and neopterin can be interpreted as a persistent but ineffective immune response. The fact that this type of immunomodulation was also found after administering leukocyte-filtered erythrocyte concentrates advocates that, in addition to the absolute leukocyte count, the length of storage and thus the viability of contaminating leukocytes plays a decisive role [6,7].…”

Section: Leukocyte Filtrationmentioning

confidence: 99%

Immunomodulation Mechanisms following Transfusion of Allogeneic und Autologous Erythrocyte Concentrates

Innerhofer¹,

Kühbacher²

2002

Transfus Med Hemother

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The residual risk of transmitting a transfusion-associated infectious disease has been considerably reduced in recent years due to improved test procedures and careful donor selection. The mortality associated with transfusion today is caused mainly by hemolytic reactions and the consequences of bacterial contamination of blood components. In addition, the effects of immunomodulation following allogeneic transfusion are not to be overlooked. Donor leukocytes, or their major histocompatibility- complex (MHC) molecules, contained in blood components stimulate above all humoral immune responses (Th2 response) in the recipient, which also causes downregulation of cellular immune responses (Th1 response). Besides the absolute leukocyte count, the length of storage of blood components, which causes a progressive apoptosis, necrosis, and secondary necrosis of leukocytes, appears to be of decisive importance. Stimulation of Th2 immune responses and suppression of Th1 immune responses results from the particular antigen presentation as is encountered for transfusions, and appears to have a causal relation to the higher incidence of postoperative infection observed in recipients of allogeneic transfusions. Contrary to the effects of allogeneic transfusions described in numerous studies, immunological responses following autologous transfusion have hardly been studied to date. Future studies will have to determine whether autologous transfusions cause not only a lack of immunosuppression but also immunostimulation.

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Immunologic changes after transfusion of autologous or allogeneic buffy coat‐poor versus WBC‐reduced blood transfusions in patients undergoing arthroplasty.II. Activation of T cells, macrophages, and cell‐mediated lympholysis

Abstract: Allogeneic transfusions seem to prolong the postoperative status of immune activation, even when WBC-filtered RBCs are used for the transfusion regimen.

Cited by 36 publications

References 25 publications

Impact of Perioperative Allogeneic Red Blood Cell Transfusion on Recurrence and Overall Survival After Resection of Colorectal Liver Metastases

Impact of Perioperative Allogeneic Red Blood Cell Transfusion on Recurrence and Overall Survival After Resection of Colorectal Liver Metastases

Low T3 Syndrome in Head-Injured Patients is Associated with Prolonged Suppression of Markers of Cell-Mediated Immune Response

Immunomodulation Mechanisms following Transfusion of Allogeneic und Autologous Erythrocyte Concentrates

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