PMID- 27798418
OWN - NLM
STAT- MEDLINE
DCOM- 20180403
LR  - 20181202
IS  - 1531-6971 (Electronic)
IS  - 1070-5287 (Linking)
VI  - 23
IP  - 1
DP  - 2017 Jan
TI  - T2-low asthma: current approach to diagnosis and therapy.
PG  - 48-55
AB  - PURPOSE OF REVIEW: Asthma is a heterogeneous disease not only on a clinical but 
      also on a mechanistic level. For a long time, the molecular mechanisms of asthma 
      were considered to be driven by type 2 helper T cells (Th2) and eosinophilic 
      airway inflammation; however, extensive research has revealed that T2-low 
      subtypes that differ from the dominant T2 paradigm are also common. RECENT 
      FINDINGS: Research into asthma pathways has led to the recognition that some 
      asthma phenotypes show absence of T2 inflammation or alternate between T2 and 
      non-T2 responses. Moreover, numerous immune response modifiers that block 
      key-molecules such as interleukin (IL)-5, IL-13, and immunoglobulin E (IgE) have 
      been identified. Along the way, these studies pointed that T2-low inflammation 
      may also be responsible for lack of responsiveness to current treatment regimes. 
      SUMMARY: Asthma pathogenesis is characterized by two major endotypes, a T2-high 
      featuring increased eosinophilic airway inflammation, and a T2-low endotype 
      presenting with either neutrophilic or paucigranulocytic airway inflammation and 
      showing greater resistance to steroids. This clearly presents an unmet 
      therapeutic challenge. A precise definition and characterization of the 
      mechanisms that drive this T2-low inflammatory response in each patient phenotype 
      is necessary to help identify novel drug targets and design more effective and 
      targeted treatments.
FAU - Samitas, Konstantinos
AU  - Samitas K
AD  - 7th Respiratory Medicine Department and Asthma Center, Athens Chest Hospital 
      'Sotiria', Athens, Greece.
FAU - Zervas, Eleftherios
AU  - Zervas E
FAU - Gaga, Mina
AU  - Gaga M
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Opin Pulm Med
JT  - Current opinion in pulmonary medicine
JID - 9503765
RN  - 0 (Anti-Asthmatic Agents)
RN  - 0 (IL5 protein, human)
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-5)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Anti-Asthmatic Agents/therapeutic use
MH  - Asthma/diagnosis/drug therapy/*immunology
MH  - Humans
MH  - Immunoglobulin E/immunology
MH  - Inflammation/immunology
MH  - Interleukin-13/immunology
MH  - Interleukin-5/immunology
MH  - Th2 Cells/*immunology
EDAT- 2016/11/02 06:00
MHDA- 2018/04/04 06:00
CRDT- 2016/11/02 06:00
PHST- 2016/11/02 06:00 [pubmed]
PHST- 2018/04/04 06:00 [medline]
PHST- 2016/11/02 06:00 [entrez]
AID - 10.1097/MCP.0000000000000342 [doi]
PST - ppublish
SO  - Curr Opin Pulm Med. 2017 Jan;23(1):48-55. doi: 10.1097/MCP.0000000000000342.