Related Experiment Video

Updated: Jun 18, 2026

Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)
14:26

Purification of Extracellular Trypanosomes, Including African, from Blood by Anion-Exchangers (Diethylaminoethyl-cellulose Columns)

Published on: April 6, 2019

Trypanosoma carassii calreticulin binds host complement component C1q and inhibits classical complement

Ayoola Oladiran1, Miodrag Belosevic

  • 1Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.

Developmental and Comparative Immunology
|November 17, 2009
PubMed

Insights

Trypanosoma carassii uses calreticulin (CRT) to evade fish immune systems. This parasite protein binds to host complement component C1q, potentially inhibiting the host

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Trypanosoma carassii is an economically significant fish parasite employing immune evasion strategies.
  • Proteomic analysis identified excreted/secreted (ES) and surface molecules involved in host-parasite interactions.

Purpose of the Study:

  • To investigate the role of T. carassii calreticulin (CRT) in host immune evasion.
  • To characterize the interaction between parasite CRT and host immune components.

Main Methods:

  • Cloning and production of recombinant T. carassii calreticulin (rTcaCRT).
  • Generation of a polyclonal antibody against rTcaCRT.
  • Immunofluorescence assays to detect CRT localization on trypanosomes.
  • In vitro assays to assess the binding of rTcaCRT to host serum molecules, including C1q.
  • Hemolytic assays to evaluate the inhibition of complement-mediated lysis by rTcaCRT.

Main Results:

  • Calreticulin (CRT) was detected on the surface and within T. carassii.
  • Recombinant T. carassii calreticulin (rTcaCRT) bound host serum molecules, notably C1q.
  • rTcaCRT inhibited C1q-dependent lysis of sensitized sheep erythrocytes, confirming specific interaction.

Conclusions:

  • T. carassii calreticulin (CRT) is present on the parasite surface and interacts with host C1q.
  • Parasite CRT likely inhibits the host's classical complement pathway, contributing to immune evasion.
  • This interaction represents a novel immune evasion mechanism for T. carassii.

More Related Videos

Double Labeling Immunofluorescence using Antibodies from the Same Species to Study Host-Pathogen Interactions07:35

Double Labeling Immunofluorescence using Antibodies from the Same Species to Study Host-Pathogen Interactions

Published on: July 10, 2021

Chemical Cartography Approaches to Study Trypanosomatid Infection08:21

Chemical Cartography Approaches to Study Trypanosomatid Infection

Published on: January 21, 2022

Related Concept Videos

Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
American Trypanosomiasis01:22

American Trypanosomiasis

Chagas disease, or American trypanosomiasis, is a vector-borne parasitic infection caused by Trypanosoma cruzi, a flagellated protozoan (kinetoplastid) of the family Trypanosomatidae. The disease is endemic in Latin America, although cases are increasingly reported worldwide due to human migration. Transmission most commonly occurs when feces of infected triatomine bugs contaminate bite wounds or mucosal surfaces; additional routes include congenital, transfusional, transplant-related, and oral...
Antiprotozoal Agents01:21

Antiprotozoal Agents

Leishmaniasis is a widespread parasitic disease caused by several Leishmania species. It affects millions of people each year and remains a major public health problem in endemic regions. First-line treatment relies on pentavalent antimonials, including meglumine antimoniate and sodium stibogluconate. Even so, how these drugs work has not been fully clear, especially their interaction with parasite-specific biochemical pathways. One key target is trypanothione reductase (TR), an enzyme that...
Toxoplasmosis01:28

Toxoplasmosis

Toxoplasmosis, a zoonotic disease caused by the protozoan Toxoplasma gondii, poses significant public health challenges globally due to its high seroprevalence and varied clinical manifestations. As an obligate intracellular parasite, T. gondii can infect all warm-blooded vertebrates, but felids are its only definitive hosts, shedding unsporulated oocysts into the environment. Humans typically acquire the infection through ingestion of tissue cysts in undercooked meat or oocysts from...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...
Trichomoniasis01:18

Trichomoniasis

Trichomonas vaginalis is a flagellated protozoan parasite and the causative agent of trichomoniasis, one of the most prevalent non-viral sexually transmitted infections in the United States. This extracellular parasite primarily colonizes the lower genitourinary tract in women—particularly the vagina—and in men, the urethra and prostate. Its structural and functional adaptations enable its survival, motility, and pathogenicity within the host environment.Structural Features and Host EntryT.