scholarly journals Vernal keratoconjunctivitis in human immunodeficiency virus – The possible role of T-helper 1–T-helper 2 shift

2018 ◽  
Vol 66 (7) ◽  
pp. 1004 ◽  
Author(s):  
Bhaskar Srinivasan ◽  
Shweta Agarwal ◽  
Geetha Iyer ◽  
Sridharan Sudharshan ◽  
Kavita Kalaivani
Immunology ◽  
2000 ◽  
Vol 99 (1) ◽  
pp. 109-112 ◽  
Author(s):  
K. M. Gillespie ◽  
C.-C. Szeto ◽  
V. M. Betin ◽  
P. W. Mathieson

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Lynne Sykes ◽  
David A. MacIntyre ◽  
Xiao J. Yap ◽  
Tiong Ghee Teoh ◽  
Phillip R. Bennett

Pregnancy is a unique immunological state in which a balance of immune tolerance and suppression is needed to protect the fetus without compromising the mother. It has long been established that a bias from the T helper 1 cytokine profile towards the T helper 2 profile contributes towards successful pregnancy maintenance. The majority of publications that report on aberrant Th1:Th2 balance focus on early pregnancy loss and preeclampsia. Over the last few decades, there has been an increased awareness of the role of infection and inflammation in preterm labour, and the search for new biomarkers to predict preterm labour continues. In this paper, we explore the evidence for an aberrant Th1:Th2 profile associated with preterm labour. We also consider the potential for its use in screening women at high risk of preterm labour and for prophylactic therapeutic measures for the prevention of preterm labour and associated neonatal adverse outcomes.


2008 ◽  
Vol 12 (3) ◽  
pp. 126-132 ◽  
Author(s):  
Sanjeev Handa ◽  
Tarun Narang ◽  
Ajay Wanchu

Background: Dermatologic conditions are often an early clue to human immunodeficiency virus (HIV) infection. As the disease progresses and the host immunity fails, patients may develop a number of skin conditions. At this point, they have a dominant T helper 2 immunologic response. After the initiation of antiretroviral therapy, the T helper 1 response is restored, and some skin problems, paradoxically, make their appearance then. Conclusion: Herpes zoster, mucocutaneous herpes, eosinophilic folliculitis, and mycobacterial infections have been known to occur at this stage. This may be because immune restoration of a host's immunity causes recognition of silent or latent infection and results in development of the condition. We report five cases that were seen at our center during a 2-year period.


1999 ◽  
Vol 73 (1) ◽  
pp. 316-324 ◽  
Author(s):  
Youichi Suzuki ◽  
Yoshio Koyanagi ◽  
Yuetsu Tanaka ◽  
Tsutomu Murakami ◽  
Naoko Misawa ◽  
...  

ABSTRACT Cytokines are potent stimuli for CD4+-T-cell differentiation. Among them, interleukin-12 (IL-12) and IL-4 induce naive CD4+ T cells to become T-helper 1 (Th1) or Th2 cells, respectively. In this study we found that macrophage-tropic human immunodeficiency virus type 1 (HIV-1) strains replicated more efficiently in IL-12-induced Th1-type cultures derived from normal CD4+ T cells than did T-cell-line-tropic (T-tropic) strains. In contrast, T-tropic strains preferentially infected IL-4-induced Th2-type cultures derived from the same donor CD4+ T cells. Additional studies using chimeric viruses demonstrated that the V3 region of HIV-1 gp120 was the principal determinant for efficiency of replication. Cell fusion analysis showed that cells expressing envelope protein from a T-tropic strain effectively fused with IL-4-induced Th2-type culture cells. Flow cytometric analysis showed that the level of CCR5 expression was higher on IL-12-induced Th1-type culture cells, whereas CXCR4 was highly expressed on IL-4-induced Th2-type culture cells, although a low level of CXCR4 expression was observed on IL-12-induced Th1-type culture cells. These results indicate that HIV-1 isolates exhibit differences in the ability to infect CD4+-T-cell subsets such as Th1 or Th2 cells and that this difference may partly correlate with the expression of particular chemokine receptors on these cells. The findings suggest that immunological conditions are one of the factors responsible for inducing selection of HIV-1 strains.


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