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  • The American Association of Immunologists  (11)
  • Medicine  (11)
  • 1
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    Online Resource
    Acute Loss of Intestinal CD4+ T Cells Is Not Predictive of Simian Immunodeficiency Virus Virulence
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 179, No. 5 ( 2007-09-01), p. 3035-3046
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 179, No. 5 ( 2007-09-01), p. 3035-3046
    Abstract: The predictive value of acute gut-associated lymphoid tissue (GALT) CD4+ T cell depletion in lentiviral infections was assessed by comparing three animal models illustrative of the outcomes of SIV infection: pathogenic infection (SIVsmm infection of rhesus macaques (Rh)), persistent nonprogressive infection (SIVagm infection of African green monkeys (AGM)), and transient, controlled infection (SIVagm infection of Rh). Massive acute depletion of GALT CD4+ T cells was a common feature of acute SIV infection in all three models. The outcome of this mucosal CD4+ T cell depletion, however, differed substantially between the three models: in SIVsmm-infected Rh, the acute GALT CD4+ T cell depletion was persistent and continued with disease progression; in SIVagm, intestinal CD4+ T cells were partially restored during chronic infection in the context of normal levels of apoptosis and immune activation and absence of damage to the mucosal immunologic barrier; in SIVagm-infected Rh, complete control of viral replication resulted in restoration of the mucosal barrier and immune restoration. Therefore, our data support a revised paradigm wherein severe GALT CD4+ T cell depletion during acute pathogenic HIV and SIV infections of humans and Rh is necessary but neither sufficient nor predictive of disease progression, with levels of immune activation, proliferation and apoptosis being key factors involved in determining progression to AIDS.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.179.5.3035
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
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  • 2
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    Impaired Development and Expansion of Germinal Center Follicular Th Cells in Simian Immunodeficiency Virus–Infected Neonatal Macaques
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 201, No. 7 ( 2018-10-01), p. 1994-2003
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 201, No. 7 ( 2018-10-01), p. 1994-2003
    Abstract: Germinal center (GC) CD4+ follicular Th (Tfh) cells are critical for cognate B cell help in humoral immune responses to pathogenic infections. Although Tfh cells are expanded or depleted in HIV/SIV-infected adults, the effects of pediatric HIV/SIV infection on Tfh cells remain unclear. In this study, we examined changes in lymphoid follicle formation in lymph nodes focusing on GC Tfh cells, B cell development, and differentiation in SIV-infected neonatal rhesus macaques (Macaca mulatta) compared with age-matched cohorts. Our data showed that follicles and GCs of normal infants rapidly formed in the first few weeks of age, in parallel with increasing GC Tfh cells in various lymphoid tissues. In contrast, GC development and GC Tfh cells were markedly impaired in SIV-infected infants. There was a very low frequency of GC Tfh cells throughout SIV infection in neonates and subsequent infants, accompanied by high viremia, reduction of B cell proliferation/resting memory B cells, and displayed proinflammatory unresponsiveness. These findings indicate neonatal HIV/SIV infection compromises the development of GC Tfh cells, likely contributing to ineffective Ab responses, high viremia, and eventually rapid disease progression to AIDS.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1800235
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
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  • 3
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    Intestinal double positive CD4+CD8+ T cells of neonates are highly activated memory cells with higher proliferative capacity compared to single positive CD4+/CD8+ T cells (B115)
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 178, No. 1_Supplement ( 2007-04-01), p. LB24-LB24
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 1_Supplement ( 2007-04-01), p. LB24-LB24
    Abstract: Peripheral blood and thymic double positive CD4+CD8+ (DP) T cells from neonates have been described in humans and a number of animals, but the function and immunophenotypic characteristics of other tissue-derived DP T cells are not clearly understood. Here we demonstrate the phenotypic characteristics of DP cells in 6 different tissues including thymus from normal neonatal rhesus macaques (Macaca mulatta) between 0–21 days of age. In general, DP T cells of neonates have higher percentages of memory markers (CD28+CD95+, CD45RA−) compared to single positive (SP) CD4+ and CD8+ T cells. In addition, intestinal DP T cells increase as the animals’ age and levels of CD62L decrease with age suggesting that DP cells proliferate and are activated with maturity and/or antigen exposure. Consistent with this, intestinal DP T cells in neonates express higher levels of activation markers and CCR5 expression. Furthermore, DP T cells have higher rates of proliferation compared to SP CD4+ and SP CD8+ T cells as determined by BrdU labelling techniques. Finally, DP T cells produce higher levels of cytokine production in response to mitogen stimulation compared to SP CD4+ or SP CD8+ T cells. Collectively, these findings demonstrate that intestinal DP T cells of neonates are proliferating, effector cells and are likely involved in regulating immune as compared to the immature DP T cells in the thymus. As in adults, these intestinal DP T cells may be important target cells for early HIV infection in neonates due to their activation, high expression of CCR5, and memory phenotype.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.178.Supp.B115
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
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  • 4
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    Destruction of monocyte/macrophages dictate AIDS progression in SIV infected macaques (131.9)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 131.9-131.9
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 131.9-131.9
    Abstract: It is widely accepted that destruction of CD4+ T cells and viral load are the primary markers for immunodeficiency in HIV-1-infected humans and in simian immunodeficiency virus (SIV)-infected macaques. However, the mechanisms that dictate the tempo of disease progression have yet to be elucidated. Macrophages, an important cell component of the innate immune system and link between innate and adaptive immunity, are also important targets of HIV/SIV infection. We therefore examined whether changes in cells of monocyte/macrophage lineage could be linked to the pathogenesis of AIDS in the rhesus macaque model. Here we show that massive turnover of peripheral monocytes associated with death of tissue macrophages correlates with AIDS progression in macaques. More importantly, the level of monocyte turnover was not linked to the CD4+ T cell count and was a better predictive marker for AIDS progression than viral load or lymphocyte activation. Our results show the importance of monocyte/macrophages in the pathogenesis of AIDS and suggest the dynamic changes of the monocyte/macrophages as a new marker for AIDS progression.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.131.9
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
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  • 5
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    The landscape of immune responses and persistent viral reservoirs in systemic and lymphoid tissues in rhesus macaques infected by a newly developed SHIV-CH848
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 249.30-249.30
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 249.30-249.30
    Abstract: The chimeric simian/human immunodeficiency viruses (SHIVs), carrying HIV envelope glycoproteins from transmitted founder (T/F) viruses, are valuable as a challenge viruses in nonhuman primate models for validating HIV-1 vaccines, assessing viral reservoirs and latency, and developing functional “cure” strategies in HIV infection. This study comprehensively investigated immunological changes, viral replication and reservoir size in deep tissues of SHIV-CH848-infected rhesus macaques on antiretroviral therapy (cART). Material & Method A total of 10 rhesus macaques (Macaca mulatta, RMs) were intravenously (i.v.)inoculated with SHIV-CH848, containing vpu-env(gp140) sequence from T/F HIV-1 subtype C strain CH848. At 3 months post SHIV infection, 5 animals received cART for 6 months, and remaining 5 animals as untreated controls. Blood, lymph node and rectal biopsies were collected to examine plasma viral load, cell-associated viral RNA/DNA and host immune responses. Results SHIV-CH848 inoculation resulted in rapid viral replication, reaching peak viremia at 14dpi. SHIV-CH848 primary infection significantly depleted peripheral and mucosal CD4+ T cells. Also, broadly neutralizing antibodies were also not elicited up to 15 months post infection. Despite gradual recovery of CD4+ T cells after cART, the levels of integrated viral DNA in tissues remained stable throughout 6-months of cART, and rapid viral rebound was observed after ART interruption. Conclusions These findings suggest that the new SHIV strain, SHIV-CH848, is able to maintain persistent viral replication in macaques, and establish long-term viral reservoirs/latency in tissues, serving as a valuable model for HIV research.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.249.30
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
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  • 6
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    Online Resource
    Increased B7-H1 Expression on Dendritic Cells Correlates with Programmed Death 1 Expression on T Cells in Simian Immunodeficiency Virus-Infected Macaques and May Contribute to T Cell Dysfunction and Disease Progression
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 185, No. 12 ( 2010-12-15), p. 7340-7348
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 185, No. 12 ( 2010-12-15), p. 7340-7348
    Abstract: Suppression of dendritic cell (DC) function in HIV-1 infection is thought to contribute to inhibition of immune responses and disease progression, but the mechanism of this suppression remains undetermined. Using the rhesus macaque model, we show B7-H1 (programmed death [PD]-L1) is expressed on lymphoid and mucosal DCs (both myeloid DCs and plasmacytoid DCs), and its expression significantly increases after SIV infection. Meanwhile, its receptor, PD-1, is upregulated on T cells in both peripheral and mucosal tissues and maintained at high levels on SIV-specific CD8+ T cell clones in chronic infection. However, both B7-H1 and PD-1 expression in SIV controllers was similar to that of controls. Expression of B7-H1 on both peripheral myeloid DCs and plasmacytoid DCs positively correlated with levels of PD-1 on circulating CD4+ and CD8+ T cells, viremia, and declining peripheral CD4+ T cell levels in SIV-infected macaques. Importantly, blocking DC B7-H1 interaction with PD-1+ T cells could restore SIV-specific CD4+ and CD8+ T cell function as evidenced by increased cytokine secretion and proliferative capacity. Combined, the results indicate that interaction of B7-H1–PD-1 between APCs and T cells correlates with impairment of CD4+ Th cells and CTL responses in vivo, and all are associated with disease progression in SIV infection. Blockade of this pathway may have therapeutic implications for HIV-infected patients.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1001642
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
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  • 7
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    Immunodomination in the Evolution of Dominant Epitope-Specific CD8+ T Lymphocyte Responses in Simian Immunodeficiency Virus-Infected Rhesus Monkeys
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 176, No. 1 ( 2006-01-01), p. 319-328
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 176, No. 1 ( 2006-01-01), p. 319-328
    Abstract: Because the control of HIV-1 replication is largely dependent on CD8+ T lymphocyte responses specific for immunodominant viral epitopes, vaccine strategies that increase the breadth of dominant epitope-specific responses should contribute to containing HIV-1 spread. Developing strategies to elicit such broad immune responses will require an understanding of the mechanisms responsible for focusing CD8+ T lymphocyte recognition on a limited number of epitopes. To explore this biology, we identified cohorts of rhesus monkeys that expressed the MHC class I molecules Mamu-A*01, Mamu-A*02, or both, and assessed the evolution of their dominant epitope-specific CD8+ T lymphocyte responses (Gag p11C- and Tat TL8-specific in the Mamu-A*01+ and Nef p199RY-specific in the Mamu-A*02+ monkeys) following acute SIV infection. The Mamu-A*02+ monkeys that also expressed Mamu-A*01 exhibited a significant delay in the evolution of the CD8+ T lymphocyte responses specific for the dominant Mamu-A*02-restricted SIV epitope, Nef p199RY. This delay in kinetics was not due to differences in viral load kinetics or magnitude or in viral escape mutations, but was associated with the evolution of the Mamu-A*01-restricted CD8+ T lymphocyte responses to the highly dominant SIV epitopes Gag p11C and Tat TL8. Thus, the evolution of dominant epitope-specific CD8+ T lymphocyte responses can be suppressed by other dominant epitope-specific responses, and this immunodomination is important in determining the kinetics of dominant epitope-specific responses.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.176.1.319
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
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  • 8
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    Dynamic decay of viral reservoirs in systemic and lymphoid compartments of SIV-infected rhesus macaques on long-term combined antiretroviral therapy
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 249.26-249.26
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 249.26-249.26
    Abstract: By quantitative real-time/digital PCR, we here longitudinally examined dynamic decay of viral parameters (cell-associated unspliced and multiply spliced viral RNA, episomal 2-LTR circular viral DNA and integrated proviral DNA) in systemic and lymphoid tissues in SIV-infected rhesus macaques on long-term combined antiretroviral therapy (cART, up to 20 months), and evaluated reservoir size and timing of viral rebound after treatment interruption. SIV RNA or DNA copy numbers were normalized and expressed as per 106 cell equivalents. Frequencies and absolute numbers of peripheral CD4+ T cells were analyzed before and after suppressive antiretroviral therapy. Results Our results showed that suppressive ART significantly reduced levels of cell-associated unspliced and multiply spliced SIV RNA/2-LTR DNA to undetectable, yet levels of integrated proviral DNA alone were stably maintained in systemic and lymphoid compartments throughout cART, which correlated with levels of viral replication prior to initiating cART. Following ATI, rapid clonal expansion of cells with integrated provirus were detected, as indicated by undetectable spliced tat/rev RNA and 2-LTR but increased levels of total proviral DNA, which may have contributed to subsequent viral rebound. Cell-associated SIV RNA and DNA levels completely recovered to pre-treatment levels in blood, spleen, lymph node, tonsil and gut-associated lymphoid tissues by 3 months after ATI. Conclusions These findings suggest that discriminating integrated HIV proviral DNA from non-integrated or defective proviruses in tissues are useful biomarkers for monitoring HIV persistence and latency for treatment and cure strategies.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.249.26
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    Persistent Simian Immunodeficiency Virus Infection Causes Ultimate Depletion of Follicular Th Cells in AIDS
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 195, No. 9 ( 2015-11-01), p. 4351-4357
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 195, No. 9 ( 2015-11-01), p. 4351-4357
    Abstract: CD4+ T follicular helper (Tfh) cells are critical for the generation of humoral immune responses to pathogenic infections, providing help for B cell development, survival, and affinity maturation of Abs. Although CD4+ Tfh cells are reported to accumulate in HIV or SIV infection, we found that germinal center Tfh cells, defined in this study as CXCR5+PD-1HIGHCD4+ T cells, did not consistently accumulate in chronically SIV-infected rhesus macaques compared with those infected with less pathogenic simian HIV, vaccinated and SIVmac-challenged, or SIVmac-infected Mamu-A*01+ macaques, all of which are associated with some control of virus replication and slower disease progression. Interestingly, CXCR5+PD-1HIGH Tfh cells in lymphoid tissues were eventually depleted in macaques with AIDS compared with the other cohorts. Chronic activation and proliferation of CXCR5+PD-1HIGH Tfh were increased, but PD-L2 expression was downregulated on B cells, possibly resulting in germinal center Tfh cell apoptosis. Together, these findings suggest that changes in CXCR5+PD-1HIGH Tfh cells in lymph nodes correlate with immune control during infection, and their loss or dysregulation contribute to impairment of B cell responses and progression to AIDS.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1501273
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
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  • 10
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    Online Resource
    Simian Immunodeficiency Virus (SIV)-Specific CTL Are Present in Large Numbers in Livers of SIV-Infected Rhesus Monkeys
    The American Association of Immunologists ; 2000
    In:  The Journal of Immunology Vol. 164, No. 11 ( 2000-06-01), p. 6015-6019
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 164, No. 11 ( 2000-06-01), p. 6015-6019
    Abstract: The immunopathogenesis of AIDS-associated hepatitis was explored in the SIV/rhesus monkey model. The livers of SIV-infected monkeys showed a mild hepatitis, with a predominantly CD8+ T lymphocyte infiltration in the periportal fields and sinusoids. These liver-associated CD8+ T cells were comprised of a high percentage of SIV-specific CTL as defined by MHC class I/Gag peptide tetramer binding and Gag peptide epitope-specific lytic activity. There was insufficient viral replication in these livers to account for attracting this large number of functional virus-specific CTL to the liver. There was also no evidence that the predominant population of CTL were functionally end-stage cells trapped in the liver and destined to undergo apoptotic cell death in that organ. Interestingly, we noted that liver tetramer-binding cells showed an increased expression of CD62L, an adhesion molecule usually only rarely expressed on tetramer-binding cells. This observation suggests that the expression of specific adhesion molecules by CTL might facilitate the capture of these cells in the liver. These results demonstrate that functional SIV-specific CD8+ T cells are present in large numbers in the liver of chronically SIV-infected monkeys. Thus, the liver may be a trap for virus-specific cytotoxic T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.164.11.6015
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2000
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