scholarly journals Clone-specific immune reactions in a trematode-crustacean system

Parasitology ◽  
2011 ◽  
Vol 139 (1) ◽  
pp. 128-136 ◽  
Author(s):  
ANSON V. KOEHLER ◽  
ROBERT POULIN
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Microsatellite Markers ◽  
Immune Reaction ◽  
Host Immune Response ◽  
Ecological Immunology ◽  
Experimental Exposure ◽  
Immune Reactions ◽  
Essential Aspect

SUMMARYVariability of immune responses is an essential aspect of ecological immunology, yet how much of this variability is due to differences among parasite genotypes remains unknown. Here, variation in immune response of the crab, Macrophthalmus hirtipes, is examined as a function of experimental exposure to 10 clonal cercarial lineages of the trematode Maritrema novaezealandensis. Our goals were (1) to assess the variability of the host immune reaction elicited by 10 parasite clones, (2) to test if the heterozygosity–fitness correlation, whereby organisms with higher heterozygosities achieve a higher fitness than those with lower heterozygosities, applies to heterozygous parasites eliciting weak immune responses, and (3) to see how concomitant infections by other macroparasites influence the crab's immune response to cercariae. Parasite clones were distinguished and heterozygosities calculated using 20 microsatellite markers. We found that exposure to cercariae resulted in increased haemocyte counts, and that although interclonal differences in immune response elicited were detected, parasite heterozygosity did not correlate with host immune response. Additionally, the presence of other pre-existing parasites in hosts did not influence their immune response following experimental exposure to cercariae. Overall, the existence of variability in immune response elicited by different parasite clones is promising for future ecological immunology studies using this system.

scholarly journals The features of host immune response with respect to microsatellite status of colorectal cancer

2007 ◽  
Vol 15 (1-2) ◽  
pp. 5-9
Author(s):  
Attila Fenyvesi
Keyword(s):  
Colorectal Cancer ◽  
Immune Response ◽  
Immune Responses ◽  
Continuous Production ◽  
Tumor Infiltrating Lymphocytes ◽  
Host Immune Response ◽  
Genetic Alterations ◽  
Clinicopathological Characteristics ◽  
Melting Point Analysis ◽  
Peritumoral Stroma

Background: The genetic alterations in colorectal cancer (CRC) progression are determined by two separate pathways, chromosomal and microsatellite instability (MSI). The CRCs with MSI have distinct clinicopathological characteristics with pronounced tumor-associated immune responses. The aim of our study was to investigate the intensity of host immune response in CRC tissue by comparing microsatellite stable (MSS) and instable tumors. Methods: The study was performed on CRC specimens from 28 patients with MSI and compared with 30 MSS tumors. The microsatellite status was evaluated with two markers by PCR and melting point analysis. The immunostaining with anti-CD3 pan-T cell antibody was used to quantify the number of tumor infiltrating lymphocytes. The lymphocytes in peritumoral stromal and the Crohn?s-like peritumoral reaction were counted on H&E slides. Results: No significant differences were found in the average number of lymphocytes in peritumoral stroma and in clinicopathological characteristics of CRCs. The conspicuous Crohn?s-like lymphoid reactions were present in 67.86% of CRCs with MSI versus 26.66% of MSS cases. The CRCs with MSI cases carried significantly higher numbers of tumor infiltrating T-lymphocytes (13.21 versus 7.47) (p<0.0001). Conclusion: The presences of peritumoral Crohn?s-like lymphoid and intraepithelial lymphocytic reaction were intensive markers for MSI in colorectal carcinomas in our study. The peculiar genetic instability in MSI tumors may lead to a continuous production of abnormal peptides, which act as neoantigens. They could induce specific antitumor immune responses effective in limiting tumor growth and spread. Abnormal peptides are potentially promising in immunotherapy advancing and in the design of a vaccine against colorectal tumors with MSI.

scholarly journals mSphere of Influence: Role of IRGM1 in Disease Control

mSphere ◽  
2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Sumanta Kumar Naik
Keyword(s):  
Immune Response ◽  
Quality Control ◽  
Mycobacterium Tuberculosis ◽  
Immune Responses ◽  
Disease Control ◽  
Host Immune Response ◽  
Specific Interest ◽  
Mitochondrial Quality Control ◽  
Content Type

ABSTRACT Sumanta K. Naik works in the tuberculosis field, with a specific interest in the host immune response to Mycobacterium tuberculosis infection. In this mSphere of Influence article, he reflects on how the paper “IRGM1 links mitochondrial quality control to autoimmunity” by Prashant Rai et al. (Nat Immunol, 22:312–321, 2021, https://doi.org/10.1038/s41590-020-00859-0) impacted his research by revealing new roles for Irgm1 in immune responses.

scholarly journals Impact of Toll-Like Receptor-Specific Agonists on the Host Immune Response to the Yersinia pestis Plague rF1V Vaccine

2021 ◽  
Vol 12 ◽  
Author(s):  
Sergei Biryukov ◽  
Jennifer L. Dankmeyer ◽  
Zain Shamsuddin ◽  
Ivan Velez ◽  
Nathaniel O. Rill ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Fusion Protein ◽  
Yersinia Pestis ◽  
Vaccine Efficacy ◽  
Host Immune Response ◽  
Toll Like Receptor ◽  
Vaccine Strategy ◽  
Pneumonic Plague ◽  
Plague Vaccine

Relatively recent advances in plague vaccinology have produced the recombinant fusion protein F1-V plague vaccine. This vaccine has been shown to readily protect mice from both bubonic and pneumonic plague. The protection afforded by this vaccine is solely based upon the immune response elicited by the F1 or V epitopes expressed on the F1-V fusion protein. Accordingly, questions remain surrounding its efficacy against infection with non-encapsulated (F1-negative) strains. In an attempt to further optimize the F1-V elicited immune response and address efficacy concerns, we examined the inclusion of multiple toll-like receptor agonists into vaccine regimens. We examined the resulting immune responses and also any protection afforded to mice that were exposed to aerosolized Yersinia pestis. Our data demonstrate that it is possible to further augment the F1-V vaccine strategy in order to optimize and augment vaccine efficacy.

Understanding the immune responses involved in mediating protection or immunopathology during leishmaniasis

2021 ◽  
Author(s):  
Thalia Pacheco-Fernandez ◽  
Greta Volpedo ◽  
Chaitenya Verma ◽  
Abhay R. Satoskar
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Public Health Problem ◽  
Host Immune Response ◽  
Sand Fly ◽  
Leishmania Infection ◽  
Major Public Health Problem ◽  
Wide Range ◽  
Vector Borne ◽  
Leishmania Parasites

Leishmaniasis is a vector-borne Neglected Tropical Disease (NTD) transmitted by the sand fly and is a major public health problem worldwide. Infections caused by Leishmania clinically manifest as a wide range of diseases, such as cutaneous (CL), diffuse cutaneous (DCL), mucosal (MCL) and visceral leishmaniasis (VL). The host innate and adaptative immune responses play critical roles in the defense against leishmaniasis. However, Leishmania parasites also manipulate the host immune response for their survival and replication. In addition, other factors such as sand fly salivary proteins and microbiota also promote disease susceptibility and parasite spread by modulating local immune response. Thus, a complex interplay between parasite, sand fly and the host immunity governs disease severity and outcome. In this review, we discuss the host immune response during Leishmania infection and highlight the factors associated with resistance or susceptibility.

scholarly journals An AI-guided invariant signature places MIS-C with Kawasaki disease in a continuum of host immune responses

2021 ◽  
Author(s):  
Debashis Sahoo ◽  
Gajanan Dattatray ◽  
Chisato Shimizu ◽  
Jihoon Kim ◽  
Soni Khandelwal ◽  
...  
Keyword(s):  
Immune Response ◽  
Kawasaki Disease ◽  
Immune Responses ◽  
Clinical Course ◽  
Host Immune Response ◽  
Rna Sequences ◽  
Host Immune Responses ◽  
Transcript Signature ◽  
Inflammatory Syndrome ◽  
Formalin Fixed

A significant surge in cases of multisystem inflammatory syndrome in children (MIS-C, also called Pediatric Inflammatory Multisystem Syndrome - PIMS) has been observed amidst the COVID-19 pandemic. MIS-C shares many clinical features with Kawasaki disease (KD), although clinical course and outcomes are divergent. We analyzed whole blood RNA sequences, serum cytokines, and formalin fixed heart tissues from these patients using a computational toolbox of two gene signatures, i.e., the 166-gene viral pandemic (ViP) signature, and its 20-gene severe (s)ViP subset that were developed in the context of SARS-CoV-2 infection and a 13-transcript signature previously demonstrated to be diagnostic for KD. Our analyses revealed that KD and MIS-C are on the same continuum of the host immune response as COVID-19 but diverge with two different cardiac phenotypes. The ViP signatures helped unravel the nature of the host immune response (IL15-centric) in MIS-C and KD, reveal unique targetable cytokine pathways in MIS-C, place MIS-C farther along in the spectrum in severity compared to KD and pinpoint key clinical (reduced cardiac function) and laboratory (thrombocytopenia and eosinopenia) parameters that can be useful to monitor severity.

scholarly journals The host cellular immune response to infection by Campylobacter spp. and its role in disease

2021 ◽  
Author(s):  
Sean M. Callahan ◽  
Carolina G. Dolislager ◽  
Jeremiah G. Johnson
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Gastrointestinal Disease ◽  
Clinical Manifestations ◽  
Host Immune Response ◽  
Secretion Systems ◽  
Cellular Immune Responses ◽  
Gastrointestinal Pathology ◽  
Cellular Immune ◽  
Post Infectious

Campylobacter spp. are the leading cause of bacterial-derived gastroenteritis worldwide, impacting ninety-six million individuals annually. Unlike other bacterial pathogens of the gastrointestinal tract, Campylobacter spp. lack many of the classical virulence factors that are often associated with the ability to induce disease in humans, including an array of canonical secretion systems and toxins. As such, the clinical manifestations of human campylobacteriosis and its resulting gastrointestinal pathology are believed to be primarily due to the host immune response toward the bacterium. Further, while gastrointestinal infection is usually self-limiting, numerous post-infectious disorders can occur, including the development of Guillan-Barré syndrome, reactive arthritis, and irritable bowel syndrome. Because gastrointestinal disease likely results from the host immune response, the development of these post-infectious disorders may be due to dysregulation or misdirection of the same inflammatory response. As a result, it is becoming increasingly important to the Campylobacter field, and human health, that the cellular immune responses toward Campylobacter be better understood, including which immunological events are critical to the development of disease and the post-infectious disorders mentioned above. In this review, we will collectively cover the cellular immune responses across susceptible hosts to C. jejuni infection, along with the tissue pathology and post-infectious disorders which may develop.

scholarly journals Cysticercus cellulosae Regulates T-Cell Responses and Interacts With the Host Immune System by Excreting and Secreting Antigens

2021 ◽  
Vol 11 ◽  
Author(s):  
Xianmin Fan ◽  
Yue Zhang ◽  
Renhui Ouyang ◽  
Bo Luo ◽  
Lizhu Li ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Immune Responses ◽  
Cytokine Production ◽  
Host Immune Response ◽  
Interleukin 10 ◽  
Host Immune System ◽  
Cell Responses ◽  
Cysticercus Cellulosae ◽  
T Cell Immune Responses

Cysticercus cellulosae (C. cellulosae) excretes and secretes antigens during the parasitic process to regulate the host immune response; however, resulting immune response and cytokine production in the host during infection still remains unclear. We used C. cellulosae crude antigens (CAs) as controls to explore the effect of excretory secretory antigens (ESAs) on T-cell immune responses in piglets. C. cellulosae ESAs induced imbalanced CD4+/CD8+ T-cell proportions, increased the CD4+Foxp3+ and CD8+Foxp3+ T-cell frequencies, and induced lymphocytes to produce interleukin-10, which was mainly attributed to CD4+ and CD4−CD8− T cells. The ESAs also induced Th2-type immune responses. The results showed that the ability of C. cellulosae to escape the host immune attacks and establish a persistent infection may be related to host immune response regulation by the ESAs.

scholarly journals Pathogenesis of SARS-CoV-2 and Immune Response in COVID-19

2020 ◽  
Author(s):  
Mehmet Demirci ◽  
Özge Ünlü ◽  
Akın Yiğin ◽  
Fadime Yıldız Zeyrek
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Host Immune Response ◽  
Amino Acid Sequences ◽  
Receptor Binding Site ◽  
The Third ◽  
Protease Cleavage ◽  
The World ◽  
Short Time ◽  
First Time

SARS-CoV-2, which emerged in Wuhan province of China for the first time in December 2019 and spread rapidly all over the world, is still causing an epidemic. SARS-CoV-2 is the third coronavirus outbreak we encountered after SARS-CoV and MERS-CoV infections. Due to SARS-CoV and MERS-CoV infections, we have gained experience about the pathogenesis and immune responses of coronaviruses. However, studies have shown that, unlike the information derived from our experience, SARS-CoV-2 is both very infectious and its effect on cells is different. Therefore, we aimed to compile the data of the published studies on the pathogenesis of SARS-CoV-2 and the resulting host immune response. In many studies, it has been reported that not only the presence of the host ACE2 receptor is sufficient for the infection of the host cell, but also the cleavage of the structural S protein by proteases should be materialized. It has been shown that, unlike SARS-CoV-2, SARS-CoV and MERS-CoV, it contains different protease cleavage systems and amino acid sequences in the ACE2 receptor binding site. In SARS-CoV-2 infection, as reported in studies conducted up to now, Th1 and Th2-mediated cytokine and chemokine levels in the host are different than SARS-CoV infection, and also different chemokines can be upregulated compared to other CoVs. Considering that effective vaccines have not been developed for the infectious RNA viruses despite the ongoing trials for many years, in order to reveal all these differences in the pathogenesis and immune response process and to develop effective antivirals against SARS-CoV-2 within a short time. the need for comprehensive studies on host immune response is evident.

Differential Antigenic Targets of Anti-Tumor Immune Response and Selective Immunity to Stem Cell Associated Group B SOX Proteins in Preneoplastic Versus Malignant Gammopathy.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 5116-5116
Author(s):  
Radek Spisek ◽  
Lyn-Chi Chen ◽  
Matthew Scanlan ◽  
Andrew Simpson ◽  
Gerd Ritter ◽  
...  
Keyword(s):  
Immune Response ◽  
Stem Cell ◽  
Immune Responses ◽  
Significant Proportion ◽  
Host Immune Response ◽  
Antibody Detection ◽  
Igg Antibodies ◽  
Sox Proteins ◽  
Group B ◽  
Antigenic Targets

Abstract Current information about specific antigenic targets of anti-tumor immunity in humans is largely restricted to patients with cancer. In order to gain insights into the nature of antigenic targets of host immune response in preneoplasia, we screened sera of patients with preneoplastic gammopathy (MGUS, n=28), multiple myeloma (MM, n=35), and smoldering MM (SMM, n=14) for the reactivity against a panel of 84 defined tumor antigens by a serum antibody detection array (SADA). Reactivity against 22 of the antigens in this panel was detected exclusively in the sera from MGUS, SMM or MM and not in sera from normal blood donors (n=27). Overall, reactivity to one or more of the antigens in this panel was detected in 40%, 85.7% and 54.2% of MGUS, SMM and MM patients, respectively. Interestingly, the pattern of antigenic reactivity differed between cohorts. Immune responses to certain antigens (e.g. cancer-testis antigen SSX-3 or methytransferase-3) were only detected in MM or SMM, respectively. On the other hand, immune responses to SRY-like -HMG-box2 (SOX2) protein were only seen in MGUS patients. In spite of cytogenetic similarities of tumor cells, the natural history of MGUS is markedly different from that of SMM or MM. SOX2 (a member of group B SOX family) is a transcription factor known to be expressed in embryonal neural and cancer stem cells and plays an important role in stem cell self renewal and differentiation. The observed differential reactivity to SOX2 was subsequently confirmed in separate ELISA based assays. Overall, anti-SOX2 IgG antibodies were detected in 11/55 (20%) of MGUS patients but in none of the SMM (n=25) and MM (n=23) patients tested (p=0.004). Light chains-specific ELISA revealed the polyclonal character of the humoral response thus ruling out SOX2 reactivity due to the monoclonal paraprotein itself. This is also supported by the detection of anti-SOX2 IgG in patients with non-IgG gammopathies. The absence of anti-SOX2 reactivity in SMM and MM could not be explained by global impairment of humoral immunity in MM, due to the detection of comparable reactivity to tetanus toxoid as a control antigen. SOX2 reactive IgG antibodies were present at high titers in all patients. For 8 of these patients enrolled on a prospective SWOG trial, follow up samples revealed that the pattern and extent of antibody reactivity remains stable over time. Together, these data provide evidence for broad anti-tumor humoral immune response in patients with MGUS and identify group B Sox proteins (SOX2) as a specific antigenic target in a significant proportion of patients with MGUS. The finding that antigenic targets of naturally occurring host immune response in preneoplasia may differ from those in cancer has broad implications for both early detection and immune prevention of human cancer. Protective immunity may depend not just on the presence of anti-tumor immune response, but also the “stemness” of the target population.

scholarly journals Cryptococcus neoformans Rim101 Is Associated with Cell Wall Remodeling and Evasion of the Host Immune Responses

mBio ◽  
2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Teresa R. O'Meara ◽  
Stephanie M. Holmer ◽  
Kyla Selvig ◽  
Fred Dietrich ◽  
J. Andrew Alspaugh
Keyword(s):  
Immune Response ◽  
Cell Wall ◽  
Transcription Factor ◽  
Immune System ◽  
Immune Responses ◽  
Cryptococcus Neoformans ◽  
Host Immune Response ◽  
Host Immune System ◽  
Content Type ◽  
Host Pathogen

ABSTRACTInfectious microorganisms often play a role in modulating the immune responses of their infected hosts. We demonstrate thatCryptococcus neoformanssignals through the Rim101 transcription factor to regulate cell wall composition and the host-pathogen interface. In the absence of Rim101,C. neoformansexhibits an altered cell surface in response to host signals, generating an excessive and ineffective immune response that results in accelerated host death. This host immune response to therim101Δ mutant strain is characterized by increased neutrophil influx into the infected lungs and an altered pattern of host cytokine expression compared to the response to wild-type cryptococcal infection. To identify genes associated with the observed phenotypes, we performed whole-genome RNA sequencing experiments under capsule-inducing conditions. We defined the downstream regulon of the Rim101 transcription factor and determined potential cell wall processes involved in the capsule attachment defects and altered mechanisms of virulence in therim101Δ mutant. The cell wall generates structural stability for the cell and allows the attachment of surface molecules such as capsule polysaccharides. In turn, the capsule provides an effective mask for the immunogenic cell wall, shielding it from recognition by the host immune system.IMPORTANCECryptococcus neoformansis an opportunistic human pathogen that is a significant cause of death in immunocompromised individuals. There are two major causes of death due to this pathogen: meningitis due to uncontrolled fungal proliferation in the brain in the face of a weakened immune system and immune reconstitution inflammatory syndrome characterized by an overactive immune response to subclinical levels of the pathogen. In this study, we examined howC. neoformansuses the conserved Rim101 transcription factor to specifically remodel the host-pathogen interface, thus regulating the host immune response. These studies explored the complex ways in which successful microbial pathogens induce phenotypes that ensure their own survival while simultaneously controlling the nature and degree of the associated host response.

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