Evaluation of CMV-specific cellular immune response by EliSPOT assay in kidney transplant patients

Abstract

Immunological data for CMV could be used in the clinical evaluation and decision-making process, in combination with virological monitoring, in kidney transplant recipients.

Cytomegalovirus Glycoprotein B Genotype Distribution in Italian Transplant Patients

“…In this context, as CMV replication is mainly under the control of the T-cell immune response, evaluation of CMV-specific cellular immune responses, for example by Elispot assay, could be of interest. Unfortunately, at the time of specimen collection at our center, Elispot assay was routinely performed only in kidney transplant recipients [14]. Therefore, data were available only in a minority of subjects (5 out of 9 kidney transplant recipients, and 2 kidney and liver transplant recipients).…”

Persistently high-level polyomavirus BK replication in the absence of renal function abnormalities in a kidney transplant recipient

“…Elispot assay revealed the lack of polyomavirus BK-specific T-cell response, thus suggesting the failure of patient's immune-surveillance (5,6). According to PVAN definition criteria, in this patient, a presumptive diagnosis of PVAN could be made, as evidenced by a prolonged (>3 weeks) BKV viremia >10 4 copies/mL (2,9).…”

Approaches for monitoring of non virus-specific and virus-specific T-cell response in solid organ transplantation and their clinical applications

“…Indeed the latest consensus guidelines on HCMV in SOT recommended these methods as an adjunct tool to predict risk of viremia and disease [21]. The HCMV-specific cellular assays have been evaluated in different clinical scenarios: some studies have focused on the T-cell immunity in the pre-transplantation period to potentially predict subsequent viral infection or disease [82][83][84][85][86] (Table 3), many more studies have assessed HCMV-specific cellular responses after transplantation [76,[87][88][89][90][91][92][93][94][95][96][97][98] (Table 4). Few studies have assessed HCMV-specific cell-mediated immunity in large cohorts of high-risk SOT recipients (i.e., donor HCMV-seropositive/recipient HCMV-seronegative) to predict disease development [90].…”

“…Restoration of BK-specific cellular immunity by tapering the immunosuppressive therapy may prevent the evolution to allograft dysfunction. Most studies have analyzed BKV-specific T-cell responses using peptide-based (large T or small T or VP1-VP3 antigens) ELISPOT assays [112][113][114][115][116][117] (Table 6). These studies suggest that BKV DNA loads are associated with low or undetectable antigen-specific Tcell responses, while resolution of active BKV infection is correlated with recovery of BKV-specific T-cell responses.…”

“…These evidences suggest that CD4 + T cells may play an important role in the control of virus replication. BKV-specific immunity may serve as a predictive factor for the Higher BKV-specific T-cell responses in KTR with BKV-associated nephropathy compared to KTR with self-limited BKV-clearance at recovery and 6 months after recovery from BKV reactivation [115] IFN-␥ ELISPOT A peptide mix including nine peptide sequences from VP1 and large T antigen 149 KTR Episodes of viral reactivation occurred only in non-responders (<5 spots/2 × 10 5 CD3 + T cells) KTR [116] Multiparameter flow cytometry Large T, small T, VP1, VP2 and VP3 peptide pools 39 KTR (11 recovered from severe and prolonged BKV reactivation, 16 with a fast recovery from BKV reactivation, 12 without any reactivation)…”