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Activation of the Immune Deficiency Pathway in Black-legged Ticks

Researchers identify the molecule p47 as a binding partner that induces a signaling cascade to limit microbial infection


Borrelia burgdorferi, the bacteria that causes Lyme disease, in a tick

Researchers at the University of Maryland School of Medicine have identified a molecule in the immune deficiency (IMD) pathway that acts as a binding partner and helps send the signal to counteract pathogens in the black-legged tick or Ixodes scapularis. This tick is the vector for Borrelia burgdorferi and Anaplasma phagocytophilum, pathogens which cause Lyme disease and Anaplasmosis respectively. Understanding these pathways can help address these major public health concerns and develop prevention and treatment methods for these diseases.


How the IMD pathway, which leads to immune response and microbial suppression in ticks, is activated and functions is still largely undefined. In this paper, Dr. Joao Pedra of the Tick Immunity team has identified the enzymatic substrate p47 as a positive regulator of the IMD network, meaning that its presence is necessary for the IMD pathway to activate and fight infection. Conversely, disruption of p47 expression leading to a lack of p47 increased microbial colonization by Borrelia burgdorferi and Anaplasma phagocytophilum. This shows that the presence of p47 as a binding agent is key to the signaling and activation of the IMD pathway, and ultimately the tick's ability to combat microbial attacks.


Researchers highlight the importance of ticks for arthropod immunology, specifically demonstrating that p47 induces signaling within the tick IMD pathway to fight microbial infection. This work emphasizes the importance of studying ticks to discover fundamental immunological processes. Manipulating immune signaling cascades within these ticks may lead to innovative approaches to reducing the burden of tick-borne diseases.


This paper, p47 licenses activation of the immune deficiency pathway in the tick Ixodes scapularis, is published in Proceedings of the National Academy of Sciences.


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