PMID- 31251775
OWN - NLM
STAT- MEDLINE
DCOM- 20200220
LR  - 20200309
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 14
IP  - 6
DP  - 2019
TI  - Expression of suppressor of cytokine signaling 3 (SOCS3) and interleukin-6 
      (-174-G/C) polymorphism in atopic conditions.
PG  - e0219084
LID - 10.1371/journal.pone.0219084 [doi]
LID - e0219084
AB  - Hypersensitivity of the immune system is caused by elevated immunoglobulin E 
      (IgE) levels in the serum, in response to a discrete allergen leading to allergic 
      reactions. IgE-mediated inflammation is regulated by the cascade of defense 
      related signaling molecules including interleukin-6 (IL-6) that plays pivotal 
      role in the survival and maturation of mast cells during an allergic reaction. 
      IL-6 mediated defense responses are tightly regulated by Suppressor of Cytokine 
      Signaling 3 (SOCS3), an inhibitory molecules of Janus Kinase-Signal Transducers 
      and Activators of Transcription (JAK-STAT) signaling, in a negative feedback 
      mechanism. The given study focuses on the assessment of crosstalk between SOCS3 
      and IL-6 to unravel the molecular significance of SOCS3 and IL-6 in the diagnosis 
      and prognosis of allergy. The expression study of SOCS3 through real-time PCR 
      analysis revealed, a 5.9 mean fold increase in SOCS3 expression in atopic cases 
      in comparison to control cases. Moreover, IL-6 has, also, been found 
      significantly enhanced in the serum level of atopic cases (26.4 pg/ml) as 
      compared to control cases (3.686 pg/ml). Female population was found to be at a 
      higher risk to develop atopic condition than male population as females exhibited 
      higher expression of both SOCS3 and IL-6 than males. Furthermore, the polymorphic 
      study of IL-6 promoter region (IL-6 174-G/C) in atopic population has reasserted 
      the importance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. 
      Expression of SOCS3 and IL-6 serum levels were found to be highly correlated. 
      Therefore establishing the role of IL-6 (-174-G/C) polymorphism on the expression 
      of SOCS3 and IL-6 in atopic cases. Notably, the study established SOCS3 and IL-6 
      as potential targets for the diagnosis/prognosis of allergy and for the 
      development of reliable therapeutic strategies to control atopic conditions in 
      the near future.
FAU - Jannat, Arooma
AU  - Jannat A
AD  - Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of 
      Sciences and Technology (NUST), Islamabad, Pakistan.
FAU - Khan, Maryam
AU  - Khan M
AUID- ORCID: 0000-0001-6103-1415
AD  - Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of 
      Sciences and Technology (NUST), Islamabad, Pakistan.
FAU - Shabbir, Maria
AU  - Shabbir M
AD  - Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of 
      Sciences and Technology (NUST), Islamabad, Pakistan.
FAU - Badshah, Yasmin
AU  - Badshah Y
AUID- ORCID: 0000-0002-7136-8828
AD  - Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of 
      Sciences and Technology (NUST), Islamabad, Pakistan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190628
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Interleukin-6)
RN  - 0 (Suppressor of Cytokine Signaling 3 Protein)
SB  - IM
MH  - Adult
MH  - Case-Control Studies
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Hypersensitivity/*diagnosis/genetics
MH  - Interleukin-6/*genetics
MH  - Male
MH  - Middle Aged
MH  - *Polymorphism, Single Nucleotide
MH  - Promoter Regions, Genetic
MH  - Sex Factors
MH  - Suppressor of Cytokine Signaling 3 Protein/*genetics
MH  - Young Adult
PMC - PMC6599118
COIS- The authors have declared that no competing interests exist.
EDAT- 2019/06/30 06:00
MHDA- 2020/02/23 06:00
PMCR- 2019/06/28
CRDT- 2019/06/29 06:00
PHST- 2019/01/09 00:00 [received]
PHST- 2019/06/15 00:00 [accepted]
PHST- 2019/06/29 06:00 [entrez]
PHST- 2019/06/30 06:00 [pubmed]
PHST- 2020/02/23 06:00 [medline]
PHST- 2019/06/28 00:00 [pmc-release]
AID - PONE-D-19-00714 [pii]
AID - 10.1371/journal.pone.0219084 [doi]
PST - epublish
SO  - PLoS One. 2019 Jun 28;14(6):e0219084. doi: 10.1371/journal.pone.0219084. 
      eCollection 2019.