scholarly journals Eukaryotic heat shock proteins as molecular links in innate and adaptive immune responses: Hsp60-mediated activation of cytotoxic T cells

2001 ◽  
Vol 13 (9) ◽  
pp. 1121-1127 ◽  
Author(s):  
Solveig H. Moré ◽  
Minka Breloer ◽  
Arne von Bonin
Keyword(s):  
T Cells ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Immune Responses ◽  
Cytotoxic T Cells ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Shock Proteins

Heat Shock Proteins and Scavenger Receptors: Role in Adaptive Immune Responses

2005 ◽  
Vol 34 (3) ◽  
pp. 325-342 ◽  
Author(s):  
John G. Facciponte ◽  
Ian J. MacDonald ◽  
Xiang-Yang Wang ◽  
Hyung Kim ◽  
Masoud H. Manjili ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Immune Responses ◽  
Scavenger Receptors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Shock Proteins

scholarly journals Immune Responses in the Glaucomatous Retina: Regulation and Dynamics

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1973
Author(s):  
Valery I. Shestopalov ◽  
Markus Spurlock ◽  
Oliver W. Gramlich ◽  
Markus H. Kuehn
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Vision Loss ◽  
Retinal Ganglion ◽  
Adaptive Immune Responses ◽  
Danger Signals ◽  
Adaptive Immune ◽  
Proinflammatory Mediators ◽  
Chronic Neuroinflammation ◽  
Shock Proteins

Glaucoma is a multifactorial disease resulting in progressive vision loss due to retinal ganglion cell (RGC) dysfunction and death. Early events in the pathobiology of the disease include oxidative, metabolic, or mechanical stress that acts upon RGC, causing these to rapidly release danger signals, including extracellular ATP, resulting in micro- and macroglial activation and neuroinflammation. Danger signaling also leads to the formation of inflammasomes in the retina that enable maturation of proinflammatory cytokines such IL-1β and IL-18. Chronic neuroinflammation can have directly damaging effects on RGC, but it also creates a proinflammatory environment and compromises the immune privilege of the retina. In particular, continuous synthesis of proinflammatory mediators such as TNFα, IL-1β, and anaphylatoxins weakens the blood–retina barrier and recruits or activates T-cells. Recent data have demonstrated that adaptive immune responses strongly exacerbate RGC loss in animal models of the disease as T-cells appear to target heat shock proteins displayed on the surface of stressed RGC to cause their apoptotic death. It is possible that dysregulation of these immune responses contributes to the continued loss of RGC in some patients.

Polyclonal Responses of γδ T Cells to Heat Shock Proteins

2020 ◽  
pp. 557-569
Author(s):  
Willi Born ◽  
Mary Ann DeGroote ◽  
Fu Yang-Xin ◽  
Christina Ellis Roark ◽  
Kent Heyborne ◽  
...  
Keyword(s):  
T Cells ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Γδ T Cells ◽  
Shock Proteins

V-delta2+ gamma/delta T cells directly recognize 70-kD heat shock proteins: relevance to MS

1996 ◽  
Vol 2 (5) ◽  
pp. 250-250
Author(s):  
M Salvetti ◽  
G Ristori ◽  
P Fiori ◽  
C Buttinelli ◽  
C Fieschi ◽  
...  
Keyword(s):  
T Cells ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Gamma Delta T Cells ◽  
Gamma Delta ◽  
Shock Proteins
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