Cutting Edge: Major CD8 T Cell Response to Live Bacillus Calmette-Guérin Is Mediated by CD1 Molecules

Kawashima, Tetsuo; Norose, Yoshihiko; Watanabe, Yoshiyuki; Enomoto, Yutaka; Narazaki, Hidehiko; Watari, Eiji; Tanaka, Shigeo; Takahashi, Hidemi; Yano, Ikuya; Brenner, Michael B.; Sugita, Masahiko

doi:10.4049/jimmunol.170.11.5345

Cited by 68 publications

(62 citation statements)

References 25 publications

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“…Interleukin-8 is induced rapidly, already after the first instillation, during BCG therapy (Boer de et al, 1997). (Kawashima et al, 2003).…”

Section: Secretion Of Cytokines By Urothelial Tumour Cellsmentioning

confidence: 99%

“…Strong direct evidence for NK cell or other effector cell(s) is still lacking. The recent acknowledgement of effector cells that recognise mycobacterial (glyco)lipid antigens through nonpolymorphic MHC molecules, such as CD1, may provide new insights into the true nature of the cytolytic effector cells involved in tumour cell eradication during BCG treatment (Maksymowych and Kane, 2000;Kawashima et al, 2003).…”

Section: Secretion Of Cytokines By Urothelial Tumour Cellsmentioning

confidence: 99%

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Role of urothelial cells in BCG immunotherapy for superficial bladder cancer

2004

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Intravesical instillation of Bacillus Calmette-Guérin (BCG) is used for the treatment of superficial bladder cancer, both to reduce the recurrence rate of bladder tumour and to diminish the risk of progression. Since its first therapeutic application in 1976, major research efforts have been directed to decipher the exact mechanism of action of the BCG-associated antitumour effect. Bacillus Calmette-Guérin causes an extensive local inflammatory reaction in the bladder wall. Of this, the massive appearance of cytokines in the urine of BCG-treated patients stands out. Activated lymphocytes and macrophages are the most likely sources of these cytokines, but at present other cellular sources such as urothelial tumour cells cannot be ruled out. Bacillus Calmette-Guérin is internalised and processed both by professional antigen-presenting cells and urothelial tumour cells, resulting in an altered gene expression of these cells that accumulates in the presentation of BCG antigens and secretion of particular cytokines.

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“…Interleukin-8 is induced rapidly, already after the first instillation, during BCG therapy (Boer de et al, 1997). (Kawashima et al, 2003).…”

Section: Secretion Of Cytokines By Urothelial Tumour Cellsmentioning

confidence: 99%

Section: Secretion Of Cytokines By Urothelial Tumour Cellsmentioning

confidence: 99%

Role of urothelial cells in BCG immunotherapy for superficial bladder cancer

2004

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“…Such DCs express not only peptide antigen-loaded individually restricted class I and II MHC molecules but also speciesspeciWc CD1 molecules on their surface to present BCGderived lipid/glycolipid antigens [15,20]. Indeed, Wndings that live BCG-infected DCs can be recognized by CD1 molecule-restricted but not by class I MHC moleculerestricted CD8 + T cells [16] and that the V 2V 2 T lymphocytes response to BCG by immunization in macaques with live BCG [5] have recently been reported. Moreover, a close relationship between BCG-immunization, and NKT cell activation has also been shown [9].…”

Section: Introductionmentioning

confidence: 99%

“…The viability of bacteria was constantly >90%. The BCG preparation was divided into two equal aliquots; one incubated for 30 min at 85°C to kill the bacteria and the other left at room temperature as reported recently [16].…”

Section: Infection Of Dcs With Live or Heat-inactivated Bcgmentioning

confidence: 99%

A possible mechanism of intravesical BCG therapy for human bladder carcinoma: involvement of innate effector cells for the inhibition of tumor growth

Higuchi

Shimizu

Owaki

et al. 2009

Cancer Immunol Immunother

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Intravesical bacillus Calmette-Guerin (BCG) therapy is considered the most successful immunotherapy against solid tumors of human bladder carcinoma. To determine the actual eVector cells activated by intravesical BCG therapy to inhibit the growth of bladder carcinoma, T24 human bladder tumor cells, expressing very low levels of class I MHC, were co-cultured with allogeneic peripheral blood mononuclear cells (PBMCs) with live BCG. The proliferation of T24 cells was markedly inhibited when BCGinfected dendritic cells (DCs) were added to the culture although the addition of either BCG or uninfected DCs alone did not result in any inhibition. The inhibitory eVect was much stronger when the DCs were infected with live BCG rather than with heat-inactivated BCG. The live BCG-infected DCs secreted TNF-and IL-12 within a day and this secretion continued for at least a week, while the heat-inactivated BCG-infected DCs secreted no IL-12 and little TNF-. Such secretion of cytokines may activate innate alert cells, and indeed NKT cells expressing IL-12 receptors apparently proliferated and were activated to produce cytocidal perforin among the PBMCs when live BCGinfected DCs were externally added. Moreover, depletion of T-cells from PBMCs signiWcantly reduced the cytotoxic eVect on T24 cells, while depletion of CD8 cells did not aVect T24 cell growth. Furthermore, the innate eVectors seem to recognize MICA/MICB molecules on T24 via NKG2D receptors. These Wndings suggest the involvement of innate alert cells activated by the live BCG-infected DCs to inhibit the growth of bladder carcinoma and provide a possible mechanism of intravesical BCG therapy.

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“…Eleven were synthesized, and of these, one was recognized by CD8 + T cell obtained from infected mice. The epitope, TB10.3/10.4 [20][21][22][23][24][25][26][27][28] is a 9mer found in the homologous TB10.3 (Rv3804c) and TB10.4 (Rv0288) proteins. Hammond et al used a similar approach to perform a genome-wide screen of all 3924 ORF of M. tuberculosis for epitopes presented by HLA-B*3501 (123).…”

Section: Thementioning

confidence: 99%

Mycobacterium tuberculosis-Specific CD8+ T Cells and Their Role in Immunity

2006

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There are more cases of tuberculosis in the world today than at anytime in history. The global epidemic has generated intense interest into the immunological mechanisms that control infection. While CD4 + T cells play a critical role in host immunity to Mycobacterium tuberculosis, there is considerable interest in understanding the role of other T cell subsets in preventing disease development following infection. CD8 + T cells are required for optimum host defense following M. tuberculosis infection, which has led to investigation of how this protective effect is mediated. A critical review of recent literature regarding the role of CD8 + T cells in protective immunity to M. tuberculosis infection is now required to address the strengths and weaknesses of these studies. In this review, we evaluate the evidence that CD8 + T cells are critical in immunity to M. tuberculosis infection. We discuss the specific mycobacterial proteins that are recognized by CD8 + T cells elicited during infection. Finally, we examine the effector mechanisms of CD8 + T cells generated during infection and synthesize recent studies to consider the protective roles that these T cells serve in vivo.

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Cutting Edge: Major CD8 T Cell Response to Live Bacillus Calmette-Guérin Is Mediated by CD1 Molecules

Cited by 68 publications

References 25 publications

Role of urothelial cells in BCG immunotherapy for superficial bladder cancer

Role of urothelial cells in BCG immunotherapy for superficial bladder cancer

A possible mechanism of intravesical BCG therapy for human bladder carcinoma: involvement of innate effector cells for the inhibition of tumor growth

Mycobacterium tuberculosis-Specific CD8+ T Cells and Their Role in Immunity

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