Abstract
Background HIV infection is associated with high rates of acute rejection following kidney transplantation. The underlying mechanisms for such predisposition are incompletely understood. Pathological immune activation is a hallmark of chronic HIV infection that persists despite effective antiretroviral therapy. We hypothesized that the baseline levels of T cell activation in HIV+ candidates would correlate with their risk of acute rejection following kidney transplantation. Methods Single-center retrospective cohort analysis of HIV+ adult kidney transplants performed between October 2006 and September 2013. The frequency of CD3+ HLA-DR+ cells measured by flow cytometry served as a surrogate marker of immune activation. Patients were categorized into tertiles of activation, and the rates of biopsy-proven acute rejection were compared across groups. Results (1) Compared to matched HIV− controls, the baseline number of CD3+ HLA-DR+ cells was higher in HIV+ kidney transplant candidates. (2) Abnormally high levels of activation did not decrease with transplant-associated immunosuppression. (3) Patients categorized within the lower and middle CD3+ HLA-DR+ tertiles had higher probability of rejection during the first 3 years post-transplant compared to those in the higher activation tertile (36.9% vs. 0%; log-rank P = 0.04). Conclusions Pathological immune activation in HIV+ transplant candidates does not explain their increased susceptibility to allograft rejection. Paradoxically, those with the highest levels of immune activation seem to be less prone to rejection.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 40-43 |
| Number of pages | 4 |
| Journal | Transplant Immunology |
| Volume | 38 |
| DOIs | |
| State | Published - Sep 1 2016 |
Fingerprint
Keywords
- Acute rejection
- HIV
- HLA-DR
- Immune activation
- Kidney transplant
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Transplantation
Cite this
Influence of immune activation on the risk of allograft rejection in human immunodeficiency virus-infected kidney transplant recipients. / Lorio, Marco A.; Rosa, Rossana; Suarez, Jose F.; Ruiz, Phillip; Ciancio, Gaetano; Burke, George W; Camargo Galvis, Jose.
In: Transplant Immunology, Vol. 38, 01.09.2016, p. 40-43.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Influence of immune activation on the risk of allograft rejection in human immunodeficiency virus-infected kidney transplant recipients
AU - Lorio, Marco A.
AU - Rosa, Rossana
AU - Suarez, Jose F.
AU - Ruiz, Phillip
AU - Ciancio, Gaetano
AU - Burke, George W
AU - Camargo Galvis, Jose
PY - 2016/9/1
Y1 - 2016/9/1
N2 - Background HIV infection is associated with high rates of acute rejection following kidney transplantation. The underlying mechanisms for such predisposition are incompletely understood. Pathological immune activation is a hallmark of chronic HIV infection that persists despite effective antiretroviral therapy. We hypothesized that the baseline levels of T cell activation in HIV+ candidates would correlate with their risk of acute rejection following kidney transplantation. Methods Single-center retrospective cohort analysis of HIV+ adult kidney transplants performed between October 2006 and September 2013. The frequency of CD3+ HLA-DR+ cells measured by flow cytometry served as a surrogate marker of immune activation. Patients were categorized into tertiles of activation, and the rates of biopsy-proven acute rejection were compared across groups. Results (1) Compared to matched HIV− controls, the baseline number of CD3+ HLA-DR+ cells was higher in HIV+ kidney transplant candidates. (2) Abnormally high levels of activation did not decrease with transplant-associated immunosuppression. (3) Patients categorized within the lower and middle CD3+ HLA-DR+ tertiles had higher probability of rejection during the first 3 years post-transplant compared to those in the higher activation tertile (36.9% vs. 0%; log-rank P = 0.04). Conclusions Pathological immune activation in HIV+ transplant candidates does not explain their increased susceptibility to allograft rejection. Paradoxically, those with the highest levels of immune activation seem to be less prone to rejection.
AB - Background HIV infection is associated with high rates of acute rejection following kidney transplantation. The underlying mechanisms for such predisposition are incompletely understood. Pathological immune activation is a hallmark of chronic HIV infection that persists despite effective antiretroviral therapy. We hypothesized that the baseline levels of T cell activation in HIV+ candidates would correlate with their risk of acute rejection following kidney transplantation. Methods Single-center retrospective cohort analysis of HIV+ adult kidney transplants performed between October 2006 and September 2013. The frequency of CD3+ HLA-DR+ cells measured by flow cytometry served as a surrogate marker of immune activation. Patients were categorized into tertiles of activation, and the rates of biopsy-proven acute rejection were compared across groups. Results (1) Compared to matched HIV− controls, the baseline number of CD3+ HLA-DR+ cells was higher in HIV+ kidney transplant candidates. (2) Abnormally high levels of activation did not decrease with transplant-associated immunosuppression. (3) Patients categorized within the lower and middle CD3+ HLA-DR+ tertiles had higher probability of rejection during the first 3 years post-transplant compared to those in the higher activation tertile (36.9% vs. 0%; log-rank P = 0.04). Conclusions Pathological immune activation in HIV+ transplant candidates does not explain their increased susceptibility to allograft rejection. Paradoxically, those with the highest levels of immune activation seem to be less prone to rejection.
KW - Acute rejection
KW - HIV
KW - HLA-DR
KW - Immune activation
KW - Kidney transplant
UR - http://www.scopus.com/inward/record.url?scp=84987615788&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84987615788&partnerID=8YFLogxK
U2 - 10.1016/j.trim.2016.06.001
DO - 10.1016/j.trim.2016.06.001
M3 - Article
VL - 38
SP - 40
EP - 43
JO - Transplant Immunology
JF - Transplant Immunology
SN - 0966-3274
ER -