Estimation of a neutrophil activation marker in lichen planus patients

2021 ◽  
Author(s):  
Fathia M. Khattab ◽  
Rania Ghonaim ◽  
Mai A. Samir
Keyword(s):  
Lichen Planus ◽  
Neutrophil Activation ◽  
Activation Marker

JAK2V617F Mutation Selectively Exerts the STAT3 Pathway for Enhancing a Neutrophil Activation Marker.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1901-1901
Author(s):  
Seido Oku ◽  
Katsuto Takenaka ◽  
Kotaro Shide ◽  
Takashi Kumano ◽  
Kikushige Yoshikane ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Conflicts Of Interest ◽  
Neutrophil Activation ◽  
Myelogenous Leukemia ◽  
Jak2v617f Mutation ◽  
Wild Type ◽  
Stat3 Pathway ◽  
Nb4 Cells ◽  
Pi3k Inhibitor Ly294002 ◽  
Activation Marker

Abstract Abstract 1901 Poster Board I-924 Leukocyte alkaline phosphatase (LAP) is considered as a neutrophil activation marker. The level of LAP is quantitated as the LAP score. It is well known that patients with chronic myelogenous leukemia (CML) usually have low LAP scores, whereas those with BCR-ABL negative chronic myeloproliferative disorders (MPD) have elevated LAP scores. In CML patients, the premature release of granulocytes from the bone marrow into the peripheral blood is considered as the cause of low LAP scores. However, the reason for elevated LAP scores in BCR-ABL negative MPD patients has been unclear. An acquired JAK2V617F mutation is observed in most patients with BCR-ABL negative MPD. It has been shown that the JAK2V617F mutation induces constitutive activation of its downstream signaling pathways such as STAT3/STAT5, Ras/MAPK and PI3K pathways. We speculated that an elevated LAP score might be due to the activation of Jak2 downstream pathways through the JAK2V617F mutation. We analyzed LAP expression in BCR-ABL negative MPD patients. JAK2V617F homozygous patients had higher LAP expression than JAK2V617F heterozygous or negative patients. AG490, the Jak2 inhibitor, was shown to significantly decrease the LAP expression in neutrophils of JAK2V617F positive patients. The myeloid cell line NB4 was transfected with the JAK2V617F mutation and a wild-type Jak2 using lentivirus vectors. It was observed that the JAK2V617F mutation, but not wild-type Jak2, enhanced cell proliferation. Then the LAP expression in NB4 cells was evaluated after these cells were differentiated by all-trans retinoic acid and granulocyte colony-stimulating factor. It was observed that the JAK2V617F mutation, but not wild-type Jak2, increased LAP expression. Next, we examined which of the Jak2 downstream pathways played a major role in increasing LAP expression and prompting cell proliferation. By using MEK1/2 inhibitor U0126, PI3K inhibitor LY294002, STAT3 siRNA and STAT5 siRNA, we demonstrated that the JAK2V617F mutation primarily used the STAT3 pathway to increase LAP expression. On the other hand, the JAK2V617F mutation used the STAT5, the Ras/MAPK and the PI3K pathways, but not the STAT3 pathway, to prompt proliferation of NB4 cells. In conclusion, we obtained direct evidence that the JAK2V617F mutation induced elevation of LAP scores via the STAT3 pathway, and prompted proliferation of NB4 cells via the STAT5, the Ras/MAPK and the PI3K pathways. Our findings showed the possibility that the JAK2V617F mutation might use specific downstream pathways depending on various phenotypic manifestations of BCR-ABL negative MPD. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Thalidomide Inhibits Granulocyte Responses in Healthy Humans after Ex Vivo Stimulation with Bacterial Antigens

2001 ◽  
Vol 45 (5) ◽  
pp. 1547-1549 ◽  
Author(s):  
Nicole P. Juffermans ◽  
Annelies Verbon ◽  
Marc J. Schultz ◽  
C. Erik Hack ◽  
Sander J. H. van Deventer ◽  
...  
Keyword(s):  
Oral Dose ◽  
Single Oral Dose ◽  
Ex Vivo ◽  
Lipoteichoic Acid ◽  
Neutrophil Activation ◽  
Activation Marker ◽  
Healthy Humans ◽  
Bacterial Antigens

ABSTRACT Ingestion of thalidomide was associated with a reduction in the upregulation of the granulocyte activation marker CD11b and a reduced capacity to release elastase and lactoferrin after stimulation with lipopolysaccharide or lipoteichoic acid. A single oral dose of thalidomide attenuates neutrophil activation upon ex vivo stimulation with bacterial antigens.

scholarly journals Discovery and Validation of a Novel Neutrophil Activation Marker Associated with Obesity

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yue Pan ◽  
Jeong-Hyeon Choi ◽  
Huidong Shi ◽  
Liwen Zhang ◽  
Shaoyong Su ◽  
...  
Keyword(s):  
Neutrophil Activation ◽  
Activation Marker

The nail in lichen planus

1970 ◽  
Vol 101 (3) ◽  
pp. 264-271 ◽  
Author(s):  
N. Zaias
Keyword(s):  
Lichen Planus

Vitamin A acid in treatment of oral lichen planus

1973 ◽  
Vol 107 (2) ◽  
pp. 277-277 ◽  
Author(s):  
S. H. Gunther
Keyword(s):  
Vitamin A ◽  
Lichen Planus ◽  
Oral Lichen Planus ◽  
Vitamin A Acid ◽  
Oral Lichen

Malignant degeneration of lichen planus

1971 ◽  
Vol 104 (3) ◽  
pp. 304-307 ◽  
Author(s):  
K. Kronenberg
Keyword(s):  
Lichen Planus ◽  
Malignant Degeneration

Lichen planus limited to the nails

1969 ◽  
Vol 100 (3) ◽  
pp. 371-371 ◽  
Author(s):  
C. F. Burgoon
Keyword(s):  
Lichen Planus

Lichen-planus-like keratosis

1970 ◽  
Vol 101 (6) ◽  
pp. 705-705 ◽  
Author(s):  
A. B. Ackerman
Keyword(s):  
Lichen Planus
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