Immune Reconstitution Inflammatory Syndrome (IRIS): What pathologists should know

Nelson, Ann Marie; Manabe, Yukari C.; Lucas, Sebastian

doi:10.1053/j.semdp.2017.04.010

Cited by 25 publications

(21 citation statements)

References 73 publications

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“…The syndrome is currently classified into two forms, named paradoxical IRIS and unmasked IRIS. In paradoxical IRIS, the signs and symptoms of a pre-existing opportunistic infection, partially treated, recur, or worsen intensely despite a positive response before cART [23,24]. Unmasked IRIS is characterized by the discovery of a previously undiagnosed/latent infection.…”

Section: Introductionmentioning

confidence: 99%

“…Unmasked IRIS is characterized by the discovery of a previously undiagnosed/latent infection. In this way, the signs and symptoms of opportunistic infection do not appear initially, appearing after the introduction of cART [23,24]. IRIS has been associated with a large variety of other pathogens and autoimmune diseases [21,25,26], but mycobacterial infections are the most prevalent cause of IRIS [21,27,28].…”

Section: Introductionmentioning

confidence: 99%

“…The few Brazilian studies regarding IRIS report an estimated incidence of approximately 12%, which limits the recruitment and analysis of these individuals [31,32]. Pathogenic mechanisms involved in IRIS development have been suggested, such as antigenic load, degree of immune restoration after treatment with cART, and genetic susceptibility of the host, and there is evidence that these mechanisms can interact with each other and together cause the syndrome [23,25,33]. However, studies linking host genetics to the pathogenesis of IRIS are still scarce [34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

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Clinical and genetic markers associated with tuberculosis, HIV-1 infection, and TB/HIV-immune reconstitution inflammatory syndrome outcomes

et al. 2020

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Background: Tuberculosis (TB) and AIDS are the leading causes of infectious disease death worldwide. In some TB-HIV co-infected individuals treated for both diseases simultaneously, a pathological inflammatory reaction termed immune reconstitution inflammatory syndrome (IRIS) may occur. The risk factors for IRIS are not fully defined. We investigated the association of HLA-B, HLA-C, and KIR genotypes with TB, HIV-1 infection, and IRIS onset. Methods: Patients were divided into four groups: Group 1-TB+/HIV+ (n = 88; 11 of them with IRIS), Group 2-HIV+ (n = 24), Group 3-TB+ (n = 24) and Group 4-healthy volunteers (n = 26). Patients were followed up at INI/FIOCRUZ and HGNI (Rio de Janeiro/Brazil) from 2006 to 2016. The HLA-B and HLA-C loci were typed using SBT, NGS, and KIR genes by PCR-SSP. Unconditional logistic regression models were performed for Protection/risk estimation. Results: Among the individuals with TB as the outcome, KIR2DS2 was associated with increased risk for TB onset (aOR = 2.39, P = 0.04), whereas HLA-B*08 and female gender were associated with protection against TB onset (aOR = 0.23, P = 0.03, and aOR = 0.33, P = 0.01, respectively). Not carrying KIR2DL3 (aOR = 0.18, P = 0.03) and carrying HLA-C*07 (aOR = 0.32, P = 0.04) were associated with protection against TB onset among HIV-infected patients. An increased risk for IRIS onset was associated with having a CD8 count ≤500 cells/mm 3 (aOR = 18.23, P = 0.016); carrying the KIR2DS2 gene (aOR = 27.22, P = 0.032), the HLA-B*41 allele (aOR = 68.84, P = 0.033), the KIR2DS1 + HLA-C2 pair (aOR = 28.58, P = 0.024); and not carrying the KIR2DL3 + HLA-C1/C2 pair (aOR = 43.04, P = 0.034), and the KIR2DL1 + HLA-C1/C2 pair (aOR = 43.04, P = 0.034), Conclusions: These results suggest the participation of these genes in the immunopathogenic mechanisms related to the conditions studied. This is the first study demonstrating an association of HLA-B*41, KIR2DS2, and KIR + HLA-C pairs with IRIS onset among TB-HIV co-infected individuals.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Clinical and genetic markers associated with tuberculosis, HIV-1 infection, and TB/HIV-immune reconstitution inflammatory syndrome outcomes

et al. 2020

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“…In contrast, paradoxical IRIS occurs despite effective antimicrobial therapy because of infection deterioration caused by a host immune response to antigenic products of degenerating microbes [51]. Occurring in a wide range of infective and non-infective diseases [51][52][53][54][55][56], IRIS is documented uncommonly in KS [4,[56][57][58][59]. Major and minor diagnostic criteria have been documented for KS-associated IRIS.…”

Section: Discussionmentioning

confidence: 99%

“…Notwithstanding the defined clinical diagnostic criteria for KS-associated IRIS, the histomorphological profile thereof, especially the phenotypic and immunophenotypic spectrum of the cellular inflammatory component in IRIS lesions, is poorly Increased tumorigenic potential through cytokine release [36] • Anti-tumor role o Tumor cell lysis by reactive oxygen species, natural killer cells, antibody-dependent cell-mediated cytotoxicity [36] documented. The histomorphological features that have been briefly described include either that of the typical spindle cell reaction of KS or of an intra-tumoral mononuclear inflammatory cell infiltrate, especially of CD3-positive T-lymphocytes [8,34,56,57]. While a neutrophil-rich immune response is described in cryptococal and tuberculous IRIS reactions, it is not documented in KS, to date [53,54].…”

Section: Discussionmentioning

confidence: 99%