Immunity and Immunoregulation in Helminth Infections

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 638

Special Issue Editor


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Guest Editor
Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla 54090, Mexico
Interests: immunoregulation in parasitic diseases; helminths; dendritic cell; macrophage’s response to inflammatory stimulus; interactions between helminths and their molecules with the host; inflammatory-mediated diseases
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Special Issue Information

Dear Colleagues,

Helminth infections are a major public health problem worldwide. They are deeply rooted in human evolution and will prevail for many years to come. They can disseminate in their host in almost any tissue, from muscle to brain. Thus, it is critical to not forget about the damage they cause to the people suffering from these infections. The only way to eradicate or control such helminth infections is to increase our knowledge of them: studies on host immunity can deepen our understanding of the pathogenesis of helminth infections. On the other hand, capacities that many helminth parasites have to regulate the immune response of their hosts to remain inside them for long periods, sometimes without causing any symptoms, are well-established. This immune silence needs to be broken to generate immunity. Therefore, if we know these helminth–immunoregulatory mechanisms, we could develop vaccines against them or take advantage of such activities to modulate unwanted exacerbated immune responses.

Therefore, the goal of this Special Issue is to put together the recent findings achieved, despite the pandemic, by researchers interested in helminth infections.

This Special Issue invites either original research or review articles focused on, but not limited to, the following “hot topics” in parasitic helminths research:

  • Immunomodulation on parasitic helminth diseases;
  • Immunity to helminths;
  • Cytokines/chemokines and susceptibility or resistance to helminth infections
  • Co-infections;
  • Co-morbidities during parasitic helminth infections;
  • Signaling pathways and susceptibility to helminths;
  • Role of innate lymphoid cells (ILCs) in helminth immunity;
  • Vaccine development against helminth

Dr. Luis I. Terrazas
Guest Editor

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Keywords

  • helminths
  • cytokines
  • signaling pathways
  • co-infections
  • infections and co-morbidities
  • immunity
  • immunomodulation
  • immune checkpoints
  • pathogenesis
  • vaccines

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Published Papers (1 paper)

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Research

15 pages, 2682 KiB  
Article
Echinococcus multilocularis Calreticulin Inhibits Lectin Pathway of Complement Activation by Directly Binding to Mannose-Binding Lectin
by Yuxiao Shao, Meng Xia, Yinghui Song, Yan Yan, Xiaofang Dong, Haoran Zong, Bin Zhan, Yanhai Wang and Limei Zhao
Pathogens 2025, 14(4), 354; https://doi.org/10.3390/pathogens14040354 - 5 Apr 2025
Viewed by 342
Abstract
Alveolar Echinococcosis (AE) is a serious zoonotic disease caused by infection of Echinococcus multilocularis larvae. To survive within the host, E. multilocularis has developed a complex immune evasion mechanism including the inhibition of complement activation. This study focused on a calreticulin secreted by [...] Read more.
Alveolar Echinococcosis (AE) is a serious zoonotic disease caused by infection of Echinococcus multilocularis larvae. To survive within the host, E. multilocularis has developed a complex immune evasion mechanism including the inhibition of complement activation. This study focused on a calreticulin secreted by E. multilocularis (EmCRT) and its role in binding ability to human MBL and inhibiting MBL-mannose-mediated lectin pathway of complement activation. Results demonstrated the binding of recombinant EmCRT protein to both external and natural MBL in serum and the subsequent inhibition of MBL-mannose-initiated lectin pathway reflected by the reduced formation of complement intermediate products C3b and C4b. Fragment mapping determined that the MBL binding site was located within the S-domain of EmCRT. Combining with its role in inhibiting C1q-initiated classical complement activation in our previous study, the inhibition of MBL-mannose-initiated lectin pathway identified in this study suggests EmCRT plays an important role in the immune evasion of E. multilocularis alveolar larvae against host complement attack as a survival strategy within human tissue. This study supports the approach of using EmCRT as a good candidate for vaccine and drug development against E. multilocularis infection. Full article
(This article belongs to the Special Issue Immunity and Immunoregulation in Helminth Infections)
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