Publications by authors named "H Laude"

The invasion of reticulocytes by Plasmodium vivax merozoites is dependent on the interaction of the Plasmodium vivax Duffy Binding Protein (PvDBP) with the Duffy antigen receptor for chemokines (DARC). The N-terminal cysteine-rich region II of PvDBP (PvDBPII), which binds DARC, is a leading P. vivax malaria vaccine candidate.

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Familial adenomatous polyposis (FAP) is an inherited disease characterized by the development of large number of colorectal adenomas with high risk of evolving into colorectal tumors. Mutations of the gene is often at the origin of this disease, as well as of a high percentage of spontaneous colorectal tumors. is therefore considered a tumor suppressor gene.

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Article Synopsis
  • Mpox virus (MPXV) triggered a multi-country outbreak in 2022, leading to the use of the modified vaccinia Ankara (MVA) vaccine for prevention, although its effectiveness has not been fully understood.
  • Researchers conducted assays to measure neutralizing antibodies (NAbs) in individuals infected with MPXV or vaccinated with MVA, finding varying levels of antibodies in both groups.
  • The study revealed that MPXV is less sensitive to neutralization, yet combining it with complement improves detection of antibody responses, underscoring the role of historic smallpox vaccinations in enhancing immune response against MPXV.
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Adenomatous polyposis coli (APC) is a tumor suppressor whose mutations underlie familial adenomatous polyposis (FAP) and colorectal cancer. Although its role in intestinal epithelial cells is well characterized, APC importance in T cell biology is ill defined. APC regulates cytoskeleton organization, cell polarity, and migration in various cell types.

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  • APOBEC3 enzymes, particularly A3A and A3B, are significantly upregulated in patients with Systemic Lupus Erythematosus (SLE), especially during disease flares and with high levels of interferon-α (IFN-α).
  • This upregulation, observed in a study of 57 SLE patients, was found in 14.9% of patients with a specific genetic polymorphism that enhances A3A, and it correlates with cellular DNA damage and low lymphocyte counts.
  • The findings suggest that high levels of A3A and A3B may promote cell death and inflammation in SLE, indicating that targeting these enzymes might help alleviate symptoms and reduce the formation
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