Abstract
In the last decade, substantial progress has been made in understanding the molecular mechanisms involved in initial host responses to viral infections, and how viral recognition leads to the innate responses that ultimately shape the adaptive immune response. Viruses, including herpes simplex virus (HSV) types 1 and 2, trigger toll-like receptors (TLRs) that elicit cytokine and chemokine production. In turn, this can create local resistance and modulate T- and B-cell-mediated immunity. TLR activation by HSV-produced molecules (or other synthetic agonists) leads to the remodelling of draining lymph nodes. This enhances the screening of naïve T-cells, from which antigen-specific lymphocytes can be selected and expanded. The innate response thereby serves to direct a timely and effective acquired immune response, through the initial TLR recognition of viral pathogen-associated molecular patterns that can limit or possibly exacerbate viral pathogenesis. Recently, these findings have been exploited by strategies that utilize synthetic TLR agonists as prophylactic or therapeutic devices. Such devices prime innate immune responses, enhancing host resistance to viral infections, including experimental HSV infections.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 37-41 |
| Number of pages | 5 |
| Journal | Herpes |
| Volume | 13 |
| Issue number | 2 |
| State | Published - Aug 2006 |
| Externally published | Yes |
Fingerprint
Keywords
- Genital herpes
- Herpes infections
- Herpes simplex virus transmission
- Innate immunity
- Microbicide
- TLR agonists
- Toll-like receptors
ASJC Scopus subject areas
- Virology
- Dermatology
Cite this
Toll-like receptors, innate immunity and HSV pathogenesis. / Herbst-Kralovetz, Melissa; Pyles, Richard B.
In: Herpes, Vol. 13, No. 2, 08.2006, p. 37-41.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Toll-like receptors, innate immunity and HSV pathogenesis
AU - Herbst-Kralovetz, Melissa
AU - Pyles, Richard B.
PY - 2006/8
Y1 - 2006/8
N2 - In the last decade, substantial progress has been made in understanding the molecular mechanisms involved in initial host responses to viral infections, and how viral recognition leads to the innate responses that ultimately shape the adaptive immune response. Viruses, including herpes simplex virus (HSV) types 1 and 2, trigger toll-like receptors (TLRs) that elicit cytokine and chemokine production. In turn, this can create local resistance and modulate T- and B-cell-mediated immunity. TLR activation by HSV-produced molecules (or other synthetic agonists) leads to the remodelling of draining lymph nodes. This enhances the screening of naïve T-cells, from which antigen-specific lymphocytes can be selected and expanded. The innate response thereby serves to direct a timely and effective acquired immune response, through the initial TLR recognition of viral pathogen-associated molecular patterns that can limit or possibly exacerbate viral pathogenesis. Recently, these findings have been exploited by strategies that utilize synthetic TLR agonists as prophylactic or therapeutic devices. Such devices prime innate immune responses, enhancing host resistance to viral infections, including experimental HSV infections.
AB - In the last decade, substantial progress has been made in understanding the molecular mechanisms involved in initial host responses to viral infections, and how viral recognition leads to the innate responses that ultimately shape the adaptive immune response. Viruses, including herpes simplex virus (HSV) types 1 and 2, trigger toll-like receptors (TLRs) that elicit cytokine and chemokine production. In turn, this can create local resistance and modulate T- and B-cell-mediated immunity. TLR activation by HSV-produced molecules (or other synthetic agonists) leads to the remodelling of draining lymph nodes. This enhances the screening of naïve T-cells, from which antigen-specific lymphocytes can be selected and expanded. The innate response thereby serves to direct a timely and effective acquired immune response, through the initial TLR recognition of viral pathogen-associated molecular patterns that can limit or possibly exacerbate viral pathogenesis. Recently, these findings have been exploited by strategies that utilize synthetic TLR agonists as prophylactic or therapeutic devices. Such devices prime innate immune responses, enhancing host resistance to viral infections, including experimental HSV infections.
KW - Genital herpes
KW - Herpes infections
KW - Herpes simplex virus transmission
KW - Innate immunity
KW - Microbicide
KW - TLR agonists
KW - Toll-like receptors
UR - http://www.scopus.com/inward/record.url?scp=33748064991&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33748064991&partnerID=8YFLogxK
M3 - Article
C2 - 16895653
AN - SCOPUS:33748064991
VL - 13
SP - 37
EP - 41
JO - Herpes
JF - Herpes
SN - 0969-7667
IS - 2
ER -