抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

The repair of wounds is one of the most complex biological processes that occur during human life. After an injury, multiple biological pathways immediately become activated and are synchronized to respond. In human adults, the wound repair process commonly leads to a non-functioning mass of fibrotic tissue known as a scar. By contrast, early in gestation, injured fetal tissues can be completely recreated, without fibrosis, in a process resembling regeneration. Some organisms, however, retain the ability to regenerate tissue throughout adult life. Knowledge gained from studying such organisms might help to unlock latent regenerative pathways in humans, which would change medical practice as much as the introduction of antibiotics did in the twentieth century.

/pdf/wound-repair-and-regeneration-1rzgi7hifn.pdf

Wound repair and regeneration

Macrophages in Tissue Repair, Regeneration, and Fibrosis

The cellular and molecular mechanisms underpinning tissue repair and its failure to heal are still poorly understood, and current therapies are limited. Poor wound healing after trauma, surgery, acute illness, or chronic disease conditions affects millions of people worldwide each year and is the consequence of poorly regulated elements of the healthy tissue repair response, including inflammation, angiogenesis, matrix deposition, and cell recruitment. Failure of one or several of these cellular processes is generally linked to an underlying clinical condition, such as vascular disease, diabetes, or aging, which are all frequently associated with healing pathologies. The search for clinical strategies that might improve the body’s natural repair mechanisms will need to be based on a thorough understanding of the basic biology of repair and regeneration. In this review, we highlight emerging concepts in tissue regeneration and repair, and provide some perspectives on how to translate current knowledge into viable clinical approaches for treating patients with wound-healing pathologies.

/pdf/wound-repair-and-regeneration-mechanisms-signaling-and-3pcqcb79a0.pdf

Wound repair and regeneration: Mechanisms, signaling, and translation

Charge, Sophie B. P., and Michael A. Rudnicki. Cellular and Molecular Regulation of Muscle Regeneration. Physiol Rev 84: 209–238, 2004; 10.1152/physrev.00019.2003.—Under normal circumstances, mamma...

Cellular and Molecular Regulation of Muscle Regeneration

Ontogeny of the nerve dependence of amphibian limb regeneration

The effects of retinoic acid on cell proliferation, differentiation and patterning are thought to be mediated by the various retinoic acid receptors. Different receptor types are encoded by distinct genes (α, β, and γ), whereas various isoforms within each type are encoded by splicing variants resulting from the use of alternative promoters. The only region that differs between isoforms is the N-terminal A region containing a transcriptional activating domain. It has been proposed that these alternative A regions confer distinct activities on the receptors, thus allowing each to mediate specific effects of retinoic acid, but it has been difficult to demonstrate such isoform specificity as most cells express a number of different retinoic acid receptors. In an attempt to test whether different isoforms can mediate distinct biological effects we are focusing on retinoic-acid-dependent growth inhibition of newt limb cells. We have constructed chimaeric receptors in which the retinoic acid binding domain of each of five newt retinoic acid receptors has been replaced with a thyroid hormone (T3) binding domain. These constructs were introduced individually into cells whose growth rate was then measured in the presence of T3. The chimaeric α1 receptor mediated T3-dependent inhibition of proliferation that was comparable to that given by retinoic acid, whereas the α2 isoform had no activity in this assay, nor did the δ1A, δIB and δ2 receptors. When the A region was deleted from the α1 chimaera it remained a potent T3-dependent transcriptional activator, but no longer mediated T3-dependent growth inhibition. In contrast, when the A region of α1 was transferred to a δ chimaeric receptor, the resulting molecule was fully active in T3-dependent growth inhibition. This is the first direct evidence for isoform specificity in a biological response to retinoic acid, and demonstrates that the specificity of this response is confined to the A region.

Receptor isoform specificity in a cellular response to retinoic acid (vol 263, pg 673, 1996)

The aneurogenic limb: a puzzle in cell interactions

Limb regeneration in adult urodele amphibians proceeds by formation of a blastema at the amputation plane. This paper discusses how the blastema forms, and how its positional identity on the proximodistal axis is manifest. Retinoic acid is able to reset axial specification and there is particular interest in determining how it acts. Although limb regeneration is restricted among vertebrates to the urodeles, its mechanism poses fundamental questions in development biology.

Some current problems in amphibian limb regeneration

Identification of the mechanisms underlying cellular plasticity in salamander cells is important because these may give pointers to the restricted regenerative ability of mammals. The myofibers from salamanders are remarkable for their ability to undergo cellularization and cell-cycle re-entry during regeneration. Here, we describe a detailed method for the isolation and culture of larval salamander myofibers in numbers suitable for cellular plasticity studies. The basic protocol for isolation and purification of cells can be completed in 4 h.

Preparation of cultured myofibers from larval salamander limbs for cellular plasticity studies

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