Insulin dependent diabetes mellitus.

Lactococcus lactis as a live vector: heterologous protein production and DNA delivery systems.

Intestinal Microbiota in Early Life and Its Implications on Childhood Health.

Atherosclerosis is a chronic, multifactorial disease that starts in youth, manifests clinically later in life, and can lead to myocardial infarction, stroke, claudication, and death. Although inflammatory processes have long been known to be involved in atherogenesis, interest in this subject has grown in the past 30-40 years. Animal experiments and human analyses of early atherosclerotic lesions have shown that the first pathogenic event in atherogenesis is the intimal infiltration of T cells at arterial branching points. These T cells recognize heat shock protein (HSP)60, which is expressed together with adhesion molecules by endothelial cells in response to classic risk factors for atherosclerosis. Although these HSP60-reactive T cells initiate atherosclerosis, antibodies to HSP60 accelerate and perpetuate the disease. All healthy humans develop cellular and humoral immunity against microbial HSP60 by infection or vaccination. Given that prokaryotic (bacterial) and eukaryotic (for instance, human) HSP60 display substantial sequence homology, atherosclerosis might be the price we pay for this protective immunity, if risk factors stress the vascular endothelial cells beyond physiological conditions.

The role of heat shock proteins in atherosclerosis

G protein-coupled receptors as promising cancer targets

Oral administration of Lactococcus lactis delivered heat shock protein 65 attenuates atherosclerosis in low-density lipoprotein receptor-deficient mice.

HSP65 serves as an immunogenic carrier for a diabetogenic peptide P277 inducing anti-inflammatory immune response in NOD mice by nasal administration.

Specific antibodies elicited by a novel DNA vaccine targeting gastrin-releasing

Accumulating evidence established a positive association of anti-heat shock protein 60 (HSP60) autoantibodies and the presence of atherosclerosis. However, whether anti-P277 (HSP60 437-460) autoantibodies may lead to the pathological increase in vascular permeability, a vascular leak syndrome (VLS), is unknown. In the present study, anti-P277 immunity was effectively induced in C57BL/6 mice, causing a marked increase in VLS in both normal mice and those bearing melanoma as well. Further analysis of the pathological role of anti-P277 immunity revealed that the B-cell epitopes located in P277 played a causal role in the development of VLS. Moreover, studies on endothelial cells (ECs) showed that the anti-P277 antibodies could cross-react with HSP60, highly expressed in both normal and stressed ECs, and mediate damage to cells in the presence of complement. These data suggested that humoral immune response induced by anti-P277 immunity mediates EC damage and induces VLS. These negative effects may cast shadows on P277, used as a peptide vaccine.

Immunization with P277 induces vascular leak syndrome in C57BL/6 mice via endothelial damage.

The fusion protein of HSP65 with tandem repeats of β-hCG acting as a potent tumor vaccine in suppressing hepatocarcinoma

Lu Yong

Papers

Oral administration of Lactococcus lactis delivered heat shock protein 65 attenuates atherosclerosis in low-density lipoprotein receptor-deficient mice.

HSP65 serves as an immunogenic carrier for a diabetogenic peptide P277 inducing anti-inflammatory immune response in NOD mice by nasal administration.

Specific antibodies elicited by a novel DNA vaccine targeting gastrin-releasing

Immunization with P277 induces vascular leak syndrome in C57BL/6 mice via endothelial damage.

The fusion protein of HSP65 with tandem repeats of β-hCG acting as a potent tumor vaccine in suppressing hepatocarcinoma