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In incompatible host-pathogen interactions, damage caused by the pathogen remains restricted as a result of the plant's defensive response. Most effective is the hypersensitive reaction, in which the cells around the infection site rapidly necrose. This response is associated with a coordinated and integrated set of metabolic alterations that are instrumental in impeding further pathogen ingress, as well as in enhancing the capacity of the host to limit subsequent infection by different types of pathogens [27, 77]. Altered ion fluxes across the plant cell membrane, generation of active oxygen species, changes in the phosphorylation state of regulatory proteins and transcriptional activation of plant defense systems culminate in cell death at the site of infection, local accumulation of phytoalexins and cell wall rigidification as a result of callose, lignin and suberin deposition [31, 89]. In addition, various novel proteins are induced which are collectively referred to as ``pathogenesis-related proteins '' (PRs). These PRs, defined as proteins coded for by the host plant but induced specifically in pathological or related situations [4, 81], do not only accumulate locally in the infected leaf, but are also induced systemically, associated with the development of systemic acquired resistance (SAR) against further infection by fungi, bacteria and viruses. Induction of PRs has been found in many plant species belonging to various families [78], suggestive of a general role for these proteins in adaptation to biotic stress conditions. SAR, likewise, is a generally occurring phenomenon, that engenders an enhancement of the defensive capacity of plants in response to necrotizing infections [70]. Since some of the tobacco PRs were identified as chitinases [45] and b-1,3-glucanases [38] with potential antifungal activity, it has often been suggested that the collective set of PRs may be effective in inhibiting pathogen growth, multiplication and/or spread, and be responsible for the state of SAR [42, 65]. Originally, five main classes of PRs (PR-1-5) were characterized by both biochemical and molecular-biological techniques in tobacco [9, 80]. Thereupon, in 1994 a unifying nomenclature for PRs was proposed based on their grouping into families sharing amino acid sequences, serological relationship, and/or enzymatic or biological activity. By then 11 families (PR-1--11) were recognized and classified for tobacco and tomato [81] (cf. Table 1). Criteria used for the inclusion of new families of PRs were that (i) protein(s) must be induced by a pathogen in tissues that do not normally express the protein(s), and (ii) induced expression must have been shown to occur in at least two different plant-pathogen combinations, or expression in a single plant-pathogen combination must have been confirmed independently in diaerent laboratories.