Increased Rate of HIV-1 Entry and Its Cytopathic Effect in CD4+/CXCR4+T Cells Expressing Relatively High Levels of CD26

Callebaut, Christian; Jacotot, Étienne; Blanco, Julià; Krust, Bernard; Hovanessian, Ara G.

doi:10.1006/excr.1998.4063

Cited by 22 publications

(8 citation statements)

References 63 publications

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“…Apart from its catalytic activity, CD26 interacts with several proteins, for instance, adenosine deaminase, the tyrosine phosphatase CD45, fibronectin, collagen, the chemokine receptor CXCR4, and the HIV gp120 protein [36]. In addition to indirectly facilitating entry and the cytopathic effect of X4 HIV strains [43], which is most probably mediated via CD26-cleaved CXCL12/SDF-1 with reduced receptor (CXCR4)-binding capacity, CD26 is a major entry factor for the Middle East Respiratory Syndrome coronavirus [44]. The role of CD26 within the immune system is a combination of its exopeptidase activity and its interactions with different molecules.…”

Section: Binding And/or Cleavage Of Target Proteinsmentioning

confidence: 99%

CD26/dipeptidylpeptidase IV—chemokine interactions: double-edged regulation of inflammation and tumor biology

Mortier

Gouwy

Damme

et al. 2016

Journal of Leukocyte Biology

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Post-translational modification of chemokines is an essential regulatory mechanism to enhance or dampen the inflammatory response. CD26/dipeptidylpeptidase IV, ubiquitously expressed in tissues and blood, removes NH2-terminal dipeptides from proteins with a penultimate Pro or Ala. A large number of human chemokines, including CXCL2, CXCL6, CXCL9, CXCL10, CXCL11, CXCL12, CCL3L1, CCL4, CCL5, CCL11, CCL14, and CCL22, are cleaved by CD26; however, the efficiency is clearly influenced by the amino acids surrounding the cleavage site and although not yet proven, potentially affected by the chemokine concentration and interactions with third molecules. NH2-terminal cleavage of chemokines by CD26 has prominent effects on their receptor binding, signaling, and hence, in vitro and in vivo biologic activities. However, rather than having a similar result, the outcome of NH2-terminal truncation is highly diverse. Either no difference in activity or drastic alterations in receptor recognition/specificity and hence, chemotactic activity are observed. Analogously, chemokine-dependent inhibition of HIV infection is enhanced (for CCL3L1 and CCL5) or decreased (for CXCL12) by CD26 cleavage. The occurrence of CD26-processed chemokine isoforms in plasma underscores the importance of the in vitro-observed CD26 cleavages. Through modulation of chemokine activity, CD26 regulates leukocyte/tumor cell migration and progenitor cell release from the bone marrow, as shown by use of mice treated with CD26 inhibitors or CD26 knockout mice. As chemokine processing by CD26 has a significant impact on physiologic and pathologic processes, application of CD26 inhibitors to affect chemokine function is currently explored, e.g., as add-on therapy in viral infection and cancer.

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Section: Binding And/or Cleavage Of Target Proteinsmentioning

confidence: 99%

CD26/dipeptidylpeptidase IV—chemokine interactions: double-edged regulation of inflammation and tumor biology

Mortier

Gouwy

Damme

et al. 2016

Journal of Leukocyte Biology

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“…Hovanessian and colleagues (19) have proposed that CD26 and DPPIV enzyme activity serve as essential cofactors for HIV-1 entry, but our previous studies (20) as well as others (21,22) have shown that CD26 is not a necessary cofactor for HIV-1 infection. Although it has been shown that chemokine receptors are co-receptors for HIV infection (23)(24)(25), CD26/ DPPIV still appears to regulate HIV entry and apoptosis (20,26). Since sCD26 is present in the plasma and appears to have important immunoregulatory effects, we attempted to determine whether the plasma sCD26 levels have clinical relevance in HIV-1 infected individuals.…”

Section: Introductionmentioning

confidence: 99%

Decreased Dipeptidyl Peptidase IV Enzyme Activity of Plasma Soluble CD26 and Its Inverse Correlation with HIV-1 RNA in HIV-1 Infected Individuals

Hosono

Homma

Kobayashi

et al. 1999

Clinical Immunology

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“…CD26, the membrane antigen expressing the DPPIV activity, is expressed at the lymphocyte surface and is involved in HIV entry into CEM cells [16]. ADA also associates with membrane CD26 and has a major role in lymphocyte function.…”

Section: Spc 3 and Cell Surface Protease Activitiesmentioning

confidence: 99%

Relationships between the anti-HIV V3-derived peptide SPC3 and lymphocyte membrane properties involved in virus entry: SPC3 interferes with CXCR4

Barbouche

2000

FEMS Microbiology Letters

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SPC 3 is a multiple antigen peptide derived from the V 3 loop of human immunodeficiency virus (HIV) envelope (Env). It exerts a potent anti-HIV activity whereas it alters neither Env expression nor binding to CD 4 . Here, SPC 3 binding characteristics, its subsequent intracellular fate and the fact that it inhibited SDF 1 K binding to the lymphocyte surface provided strong arguments to conclude that it exerts its anti-HIV activity through interference with the CXCR 4 coreceptor. In contrast, it interferes with none of the other major surface proteins and mechanisms involving V 3 and implicated in infection, as shown here. This work identifies the target mechanism of SPC 3 . ß

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Increased Rate of HIV-1 Entry and Its Cytopathic Effect in CD4+/CXCR4+T Cells Expressing Relatively High Levels of CD26

Cited by 22 publications

References 63 publications

CD26/dipeptidylpeptidase IV—chemokine interactions: double-edged regulation of inflammation and tumor biology

CD26/dipeptidylpeptidase IV—chemokine interactions: double-edged regulation of inflammation and tumor biology

Decreased Dipeptidyl Peptidase IV Enzyme Activity of Plasma Soluble CD26 and Its Inverse Correlation with HIV-1 RNA in HIV-1 Infected Individuals

Relationships between the anti-HIV V3-derived peptide SPC3 and lymphocyte membrane properties involved in virus entry: SPC3 interferes with CXCR4

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