Cellular requirements for tumor-specific immunity elicited by heat shock proteins: tumor rejection antigen gp96 primes CD8+ T cells in vivo.

Udono, Heiichiro; Levey, Daniel L.; Srivastava, Pramod K.

doi:10.1073/pnas.91.8.3077

Cited by 315 publications

(182 citation statements)

References 19 publications

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“…Notably, HSP-PC complexes can induce tumor-specific immunity. (44)(45)(46) (FIGURE 3) Radiation has also been shown to have similar effects in regard to immune response. In the clinical setting, a consistent increase in serum HSP70 over the duration of a standardly fractionated course of radiation therapy for prostate cancer patients was noted.…”

Section: Heat Shock Proteinsmentioning

confidence: 98%

Hyperthermia, Radiation and Chemotherapy: The Role of Heat in Multidisciplinary Cancer Care

Hurwitz

Stauffer

2014

Seminars in Oncology

123

104

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Section: Heat Shock Proteinsmentioning

confidence: 98%

Hyperthermia, Radiation and Chemotherapy: The Role of Heat in Multidisciplinary Cancer Care

Hurwitz

Stauffer

2014

Seminars in Oncology

123

104

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“…Heat shock protein 90 in combination with tumour-specific antigens has been demonstrated to produce specific antitumour immunity (Srivastava and Das, 1984;Palladino et al, 1987;Blachere et al, 1993;Udono et al, 1994;Janetzki et al, 2000). The clinical trial being reported in this paper was initiated in 1999 to help address the issue of whether treating MRCC patients with the autologous HSP90 product vitespen induces an antitumour response, and whether subcutaneous outpatient IL-2 can convert vitespen nonresponders into responders.…”

Section: Vaccination Of Metastatic Rcc Patients E Jonasch Et Almentioning

confidence: 99%

“…Heat shock proteins (HSPs) are intra-and extracellular chaperones associated with stress response (Udono et al, 1994). Exogenous antigens chaperoned by a HSP can be channelled into the endogenous pathway, presented by MHC class I molecules, and recognised by CD8 þ T lymphocytes (Suto and Srivastava, 1995).…”

mentioning

confidence: 99%

Vaccination of metastatic renal cell carcinoma patients with autologous tumour-derived vitespen vaccine: clinical findings

et al. 2008

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The aim of this study was to evaluate the clinical efficacy as determined by time to progression and response rate (RR) of autologous vitespen (formerly HSPPC-96; Oncophage, Antigenics Inc., New York, NY, USA) with and without interleukin-2 (IL-2; Proleukin: Chiron, Emoryville, CA, USA) in stage IV metastatic renal cell carcinoma (RCC) patients undergoing nephrectomy. Eighty-four patients were enrolled on study, and then underwent nephrectomy and harvest of tumour tissue for use in autologous vaccine manufacture. Initial treatment schedule started approximately 4 weeks after surgery and consisted of six injections: once weekly for 4 weeks, then two injections biweekly (vaccines administered at weeks 1, 2, 3, 4, 6, 8), followed by restaging at or around week 10. Patients who had stable or responsive disease continued to receive vaccine, with four more vaccinations biweekly (at weeks 10, 12, 14, 16). Patients who had progressive disease at week-10 evaluation received four consecutive 5-day-per-week courses of 11 × 10 6 U of IL-2 subcutaneously (weeks 10, 11, 12, 13), with four doses of vitespen at 2-week intervals (at weeks 10, 12, 14, 16). At the next evaluation (week 18), patients with a complete response received two further cycles of vitespen (with IL-2 if also received during prior cycle) or until vaccine supply was exhausted. Patients with stable disease or partial response repeated their prior cycle of therapy. Disease progressors who had not yet received IL-2 began IL-2 treatment, and progressors who had already received IL-2 came off study. Of 60 evaluable patients, 2 demonstrated complete response (CR), 2 showed partial response (PR), 7 showed stable disease, and 33 patients progressed. Sixteen patients had unconfirmed stable disease. Two patients who progressed on vaccine alone experienced disease stabilisation when IL-2 was added. Treatment with vitespen did not result in a discernable benefit in the majority of patients with metastatic RCC treated in this study. Use in combination with immunoregulatory agents may enhance the efficacy of vitespen.

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“…Heat shock proteins stimulates cell surface receptors like CD91 [61] on antigen presenting cells and results in MHC class I mediated CD8? cell meditated immunity [62]. They also stimulate innate immunity and activate dendritic cells and natural killer cells by binding with CD40, TLR-2, TLR-4, CD14 and, scavenging receptor-A [63][64][65][66].…”

Section: Therapeutic Potential Of Heat Shock Proteinsmentioning

confidence: 99%

Role of Heat Shock Proteins in Diseases and Their Therapeutic Potential

Kaul

Thippeswamy

2011

Indian J Microbiol

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Heat shock proteins are ubiquitously expressed intracellular proteins and act as molecular chaperones in processes like protein folding and protein trafficking between different intracellular compartments. They are induced during stress conditions like oxidative stress, nutritional deficiencies and radiation. They are released into extracellular compartment during necrosis. However, recent research findings highlights that, they are not solely present in cytoplasm, but also released into extracellular compartment during normal conditions and even in the absence of necrosis. When present in extracellular compartment, they have been shown to perform various functions like antigen presentation, intercellular signaling and induction of pro-inflammatory cytokines. Heat shock proteins represents as dominant microbial antigens during infection. The phylogenetic similarity between prokaryotic and eukaryotic heat shock proteins has led to proposition that, microbial heat shock proteins can induce self reactivity to host heat shock proteins and result in autoimmune diseases. The self-reactivity of heat shock proteins protects host against disease by controlling induction and release of pro-inflammatory cytokines. However, antibodies to self heat shock proteins haven been implicated in pathogenesis of autoimmune diseases like arthritis and atherosclerosis. Some heat shock proteins are potent inducers of innate and adaptive immunity. They activate dendritic cells and natural killer cells through toll-like receptors, CD14 and CD91. They play an important role in MHC-antigen processing and presentation. These immune effector functions of heat shock proteins are being exploited them as therapeutic agents as well as therapeutic targets for various infectious diseases and cancers.

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Cellular requirements for tumor-specific immunity elicited by heat shock proteins: tumor rejection antigen gp96 primes CD8+ T cells in vivo.

Cited by 315 publications

References 19 publications

Hyperthermia, Radiation and Chemotherapy: The Role of Heat in Multidisciplinary Cancer Care

Hyperthermia, Radiation and Chemotherapy: The Role of Heat in Multidisciplinary Cancer Care

Vaccination of metastatic renal cell carcinoma patients with autologous tumour-derived vitespen vaccine: clinical findings

Role of Heat Shock Proteins in Diseases and Their Therapeutic Potential

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