Inflammatory signaling plays a pivotal role in the complex scenario of the blood cell interplay with the microenvironment. It is known how inflammation regulates the hematopoietic stem cell fate, affecting its proliferation, differentiation, and self-renewal abilities. On the other hand, the blood disease itself or particular therapeutic approaches can represent an inflammatory stimulus, playing a significant role in disease progression and establishing a vicious circle, all to be explored. Furthermore, in the last years, a growing interest is emerging in the possible interplay between chronic inflammation, aging, and hematological malignancies. However, to date, many unresolved issues remain.
In some circumstances, the relationship between inflammation and the disease onset is clearly described and each player takes a specific role; other times it is not clear if the first cause the latter or vice-versa. Several cellular and molecular mechanisms are involved in this interchange; between them, in the last years, many studies focused on clonal hematopoiesis onset in multiple physio-pathological (even not hematological) conditions.
A growing body of evidence suggests a correlation between inflammation and clonal hematopoiesis. Conversely, an inflammatory state may favor the selection and emergence of a mutated hematopoietic clone; on the other hand, the mutated clone itself may increase the expression of inflammatory genes in innate immune cells. These recent findings paint a fascinating and incomplete picture of the intricate interaction between inflammation and hematopoiesis. The issue has not gone away.
The present Research Topic aims to debate the role of inflammation in blood diseases in the light of the most recent findings. All types of contributions, clarifying the impact of new or well-known mechanisms, are welcome: disease-microenvironment crosstalk, immune cells activity, and cytokines production, onset and effects of clonal hematopoiesis, the role of chronic inflammation, new inflammatory indicators, and more genetic markers description. A particular point of interest is new data impacting disease outcomes and opening new scenarios for clinical practice and diseases management.
Intriguing perspectives will emerge from this widely studied topic but even offer fascinating open questions.
Note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
Inflammatory signaling plays a pivotal role in the complex scenario of the blood cell interplay with the microenvironment. It is known how inflammation regulates the hematopoietic stem cell fate, affecting its proliferation, differentiation, and self-renewal abilities. On the other hand, the blood disease itself or particular therapeutic approaches can represent an inflammatory stimulus, playing a significant role in disease progression and establishing a vicious circle, all to be explored. Furthermore, in the last years, a growing interest is emerging in the possible interplay between chronic inflammation, aging, and hematological malignancies. However, to date, many unresolved issues remain.
In some circumstances, the relationship between inflammation and the disease onset is clearly described and each player takes a specific role; other times it is not clear if the first cause the latter or vice-versa. Several cellular and molecular mechanisms are involved in this interchange; between them, in the last years, many studies focused on clonal hematopoiesis onset in multiple physio-pathological (even not hematological) conditions.
A growing body of evidence suggests a correlation between inflammation and clonal hematopoiesis. Conversely, an inflammatory state may favor the selection and emergence of a mutated hematopoietic clone; on the other hand, the mutated clone itself may increase the expression of inflammatory genes in innate immune cells. These recent findings paint a fascinating and incomplete picture of the intricate interaction between inflammation and hematopoiesis. The issue has not gone away.
The present Research Topic aims to debate the role of inflammation in blood diseases in the light of the most recent findings. All types of contributions, clarifying the impact of new or well-known mechanisms, are welcome: disease-microenvironment crosstalk, immune cells activity, and cytokines production, onset and effects of clonal hematopoiesis, the role of chronic inflammation, new inflammatory indicators, and more genetic markers description. A particular point of interest is new data impacting disease outcomes and opening new scenarios for clinical practice and diseases management.
Intriguing perspectives will emerge from this widely studied topic but even offer fascinating open questions.
Note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
