Aging and disease

ISOAD Become a Member Search

X

Advanced Search

Table of Content

10 September 2014. VOL 5, ISSUE 5 Previous Issue Next Issue

Ischemic Stroke: A Consequence of a Diseased Immune System?
Taura L. Barr, James Simpkins

2014, 5 (5): 292-293 | DOI: 10.14336/AD.2014.0500292
Cytokines: Their Role in Stroke and Potential Use as Biomarkers and Therapeutic Targets
Danielle N. Doll, Taura L. Barr, James W. Simpkins

2014, 5 (5): 294-306 | DOI: 10.14336/AD.2014.0500294
The Immune Response to Acute Focal Cerebral Ischemia and Associated Post-stroke Immunodepression: A Focused Review
Bolanle M. Famakin

2014, 5 (5): 307-326 | DOI: 10.14336/AD.2014.0500307
Catecholamines, Steroids and Immune Alterations in Ischemic Stroke and Other Acute Diseases
Juliane Schulze, Antje Vogelgesang, Alexander Dressel

2014, 5 (5): 327-339 | DOI: 10.14336/AD.2014.0500327
17β-Estradiol and Inflammation: Implications for Ischemic Stroke
Ashley B. Petrone, James W. Simpkins, Taura L. Barr

2014, 5 (5): 340-345 | DOI: 10.14336/AD.2014.0500340
Epigenetics and Social Context: Implications for Disparity in Cardiovascular Disease
Karen L. Saban, Herbert L. Mathews, Holli A. DeVon, Linda W. Janusek

2014, 5 (5): 346-355 | DOI: 10.14336/AD.2014.0500346

Cover Illustration

10 September 2014. Vol.5 No.5
The immune response to focal cerebral ischemia: 1) Focal cerebral ischemia secondary to thrombotic or embolic event. 2) Injury to neurovascular unit resulting in either death or injury to endothelial cells, neurons, microglia etc. 3) Release of DAMPs from injured and dead neurovascular unit components resulting in innate immune activation via TLRs, RAGE and purinergic receptors on microglia and other APCs. 4) Innate immune activation leading to inflammasome activation; Signal 1= expression of pro-IL-1β and pro-IL-18. 5) Inflammasome activation; Signal 2= activation of caspase 1 and production of mature IL-1β and IL-18. 6) Production of other cytokine via NF-kB activation leading to endothelial cell and macrophage activation as well as activation of other transitional immune effector such as γδ T cells. 7) Activation of other transitional immune effectors such as immature DC, via DAMPs, and surface TLRs and migration of these immature DCs to regional lymph nodes resulting in activation of the adaptive immune response 8) Activation and differentiation of B cells. 9) Activation and differentiation of T cells. 10) Models of stroke-induced immunodepression via beta adrenergic or Th1-mediated mechanisms. BBB, Blood brain barrier; CD200R, CD200 receptor; DAMP, Danger associated molecular pattern; HMGB1, High mobility group box 1; RAGE, Receptor for advanced glycation end products; MyD88, Myeloid differentiation primary response gene 88; ASC, Apoptosis-associate speck-like protein containing a CARD (Caspase activation and recruitment domain); IL, Interleukin; DC, Dendritic cell; TCR, T cell receptor; MHC, Major histocompatibility complex, CD, Cell differentiation; Treg, T regulatory; Th, T helper; TGF, Transforming growth factor; TR1, Type 1 regulatory T cell; CNS, Central nervous system; NK, Natural killer; MBP, Myelin basic protein.

[Detail]

Cover Illustration

The immune response to focal cerebral ischemia: 1) Focal cerebral ischemia secondary to thrombotic or embolic event. 2) Injury to neurovascular unit resulting in either death or injury to endothelial cells, neurons, microglia etc. 3) Release of DAMPs from injured and dead neurovascular unit components resulting in innate immune activation via TLRs, RAGE and purinergic receptors on microglia and other APCs. 4) Innate immune activation leading to inflammasome activation; Signal 1= expression of pro-IL-1β and pro-IL-18. 5) Inflammasome activation; Signal 2= activation of caspase 1 and production of mature IL-1β and IL-18. 6) Production of other cytokine via NF-kB activation leading to endothelial cell and macrophage activation as well as activation of other transitional immune effector such as γδ T cells. 7) Activation of other transitional immune effectors such as immature DC, via DAMPs, and surface TLRs and migration of these immature DCs to regional lymph nodes resulting in activation of the adaptive immune response 8) Activation and differentiation of B cells. 9) Activation and differentiation of T cells. 10) Models of stroke-induced immunodepression via beta adrenergic or Th1-mediated mechanisms. BBB, Blood brain barrier; CD200R, CD200 receptor; DAMP, Danger associated molecular pattern; HMGB1, High mobility group box 1; RAGE, Receptor for advanced glycation end products; MyD88, Myeloid differentiation primary response gene 88; ASC, Apoptosis-associate speck-like protein containing a CARD (Caspase activation and recruitment domain); IL, Interleukin; DC, Dendritic cell; TCR, T cell receptor; MHC, Major histocompatibility complex, CD, Cell differentiation; Treg, T regulatory; Th, T helper; TGF, Transforming growth factor; TR1, Type 1 regulatory T cell; CNS, Central nervous system; NK, Natural killer; MBP, Myelin basic protein.