Identification of RANTES, MIP-1α, and MIP-1β as the Major HIV-Suppressive Factors Produced by CD8+ T Cells

@article{Cocchi1995IdentificationOR,
  title={Identification of RANTES, MIP-1$\alpha$, and MIP-1$\beta$ as the Major HIV-Suppressive Factors Produced by CD8+ T Cells},
  author={Fiorenza Cocchi and Anthony L. Devico and Alfredo Garzino-Demo and Suresh Kumar Arya and Robert C. Gallo and Paolo Lusso},
  journal={Science},
  year={1995},
  volume={270},
  pages={1811 - 1815}
}
Evidence suggests that CD8+ T lymphocytes are involved in the control of human immunodeficiency virus (HIV) infection in vivo, either by cytolytic mechanisms or by the release of HIV-suppressive factors (HIV-SF). The chemokines RANTES, MIP-1α, and MIP-1β were identified as the major HIV-SF produced by CD8+ T cells. Two active proteins purified from the culture supernatant of an immortalized CD8+ T cell clone revealed sequence identity with human RANTES and MIP-1α. RANTES, MIP-1α, and MIP-1… 
Anti-MIP-1α and Anti-RANTES Antibodies: New Allies of HIV-1?
TLDR
It is speculated that the higher activities of anti-MIP-1α and anti-RANTES antibodies in asymptomatic HIV-1 infected individuals might be due to a cross-reaction of β-chemokines with anti-V3-loop antibodies raised against gp120 of macrophage-tropic HIV- 1 strains.
Natural killer cells from HIV-1+ patients produce C-C chemokines and inhibit HIV-1 infection.
TLDR
It is demonstrated that monokine-activated NK cells, isolated from both normal and HIV-1+ donors, produce similar amounts of MIP-1alpha, Mip-1beta, and RANTES protein, in vitro, which indicate that NK cells from normal andAIDS donors produce C-C chemokines and other unidentified factors that can inhibit both macrophage- and T cell-tropic HIV- 1 replication in vitro.
Higher macrophage inflammatory protein (MIP)-1α and MIP-1β levels from CD8+ T cells are associated with asymptomatic HIV-1 infection
TLDR
The high β-chemokine-mediated anti-HIV activity was against the macrophage tropic isolate HIV-1BAL, with no demonstrable effect on the replication of the T-cell tropic HIV-2IIIB.
Inhibition of HIV Type 1 BaL Replication by MIP-lα, MIP-1β, and RANTES in Macrophages
TLDR
The results indicate that in MDMs both RANTES and IFN affect early steps of HIV-1 BaL replication, preceding the completion of viral DNA synthesis.
Secretion of MIP-1β and MIP-1α by CD8(+) T-lymphocytes correlates with HIV-1 inhibition independent of coreceptor usage.
TLDR
A multifactorial cytokine profile of CD8(+) T-lymphocytes capable of mediating noncytolytic suppression of CXCR4-tropic HIV-1 replication is defined.
Role of MIP-1β and RANTES in HIV-1 infection of microglia: inhibition of infection and induction by IFNβ
TLDR
The presence of endogenous chemokines that act as endogenous inhibitors of HIV-1 infection in microglia are demonstrated and the possibility that type I interferon can down-modulate microglial HIV- 1 infection in vivo by multiple mechanisms is suggested.
Soluble CD40 ligand induces beta-chemokine production by macrophages and resistance to HIV-1 entry.
TLDR
It is reported here that treating monocyte-derived macrophages (MDM) with a trimeric soluble form of CD40L (CD40LT) induced them to secrete high levels of the beta-chemokines RANTES, Mip-1alpha and MIP-1beta that are ligands for CCR5 and able to inhibit HIV-1 entry.
CD8+ T-cell-derived soluble factor(s), but not β-chemokines RANTES, MIP-1α, and MIP-1β, suppress HIV-1 replication in monocyte/macrophages
TLDR
The results suggest that HIV-suppressor activity of CD8+ T cells is a multifactorial phenomenon, and that RANTES, MIP-1α, and Mip-1β do not account for the entire scope of CD 8+ T-cell-derived HIV-Suppressor factors.
Endogenous Production of β-Chemokines by CD4+, but Not CD8+, T-Cell Clones Correlates with the Clinical State of Human Immunodeficiency Virus Type 1 (HIV-1)-Infected Individuals and May Be Responsible for Blocking Infection with NonSyncytium-Inducing HIV-1 In Vitro
TLDR
Results indicate that CD4+ cells can be protected against NSI-HIV-1 infection in culture through endogenously produced factors, including β-chemokines, and that β-chemicalokine production by CD4+, but not CD8+, T cells may constitute one mechanism of disease-free survival for HIV-1-infected individuals.
CD8+ cells in HIV infection produce macrophage inflammatory protein-1 alpha and RANTES: a comparative study in long-term survivors and progressor patients.
TLDR
It is suggested that resistance to HIV-1 progression in LTS may not be associated with high levels of RANTES and MIP-1 alpha production, as well as from HIV+ patients with progressive disease.
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