This disclosure provides microbes engineered to detect virulent and spore states of pathogens and release an appropriate therapeutic response accordingly and compositions and methods of use of the same.

The invention relates to immunogenic peptides comprising T-cell epitopes and oxidoreductase motifs comprising a modified cysteine, and their use in regulating the immune response in subjects.

The invention relates to immunogenic peptides comprising T-cell epitopes and oxidoreductase motifs comprising a modified cysteine, and their use in regulating the immune response in subjects.

Provided are an enzyme complex for decomposing polyethylene terephthalate (PET), a method for decomposing waste plastic using the enzyme complex, and a manufacturing method of the enzyme complex. According to the present disclosure, since the enzyme complex is a complex form of Ideonella sakaiensis-derived PETase and Candida Antarctica-derived lipase (CALB) by dockerin-cohesin binding and is simultaneously applicable to a substrate to be decomposed, it is possible to exhibit a synergistic effect on the decomposition of polyethylene terephthalate. In addition, it is possible to provide a stable enzyme complex of decomposing polyethylene terephthalate by providing a mini-scaffolding protein obtained by miniaturizing cellulosome as a scaffolding protein. In particular, the mini-scaffolding protein includes an A-type CBM3 module as a carbohydrate binding module to increase the accessibility to polyethylene terephthalate, a substrate to be decomposed, and to have quickly and efficiently polyethylene terephthalate decomposition activity.

Described herein are recombinant Clostridium botulinum neurotoxins comprising a light chain of a Clostridium botulinum neurotoxin, wherein the light chain comprises a mutation that causes minimal structural interference to the light chain protease; a heavy chain of a Clostridium botulinum neurotoxin, wherein the light and heavy chains are linked by a disulfide bond. The recombinant Clostridium botulinum neurotoxin has a 2-20 fold reduced toxicity compared to wild type Clostridium botulinum neurotoxin. Also described is a treatment method.

Disclosed herein, in some embodiments, are vectors encoding biosynthetic enzymes from gut microbiome-derived bacterium (e.g., Clostridia enzymes), engineered cells comprising the vectors, and methods of using biosynthetic enzymes from gut microbiome-derived bacterium (e.g., Clostridia enzymes) to produce fatty acid amides.

The present invention provides a method and a pharmaceutical composition for the treatment of the NDO comprising the viral expression vector carrying a transcription cassette that harbors transgene(s) inhibiting/silencing neurotransmission or synaptic transmission of afferent neurons.

The specification discloses Clostridial toxins or Clostridial toxin chimeras comprising an inactivation cleavage site, polynucleotide molecules encoding such toxins or chimeras, compositions comprising such toxins or chimeras, and method of producing such toxins or chimeras.

The specification discloses Clostridial toxins or Clostridial toxin chimeras comprising an inactivation cleavage site, polynucleotide molecules encoding such toxins or chimeras, compositions comprising such toxins or chimeras, and method of producing such toxins or chimeras.

Pre-conditioning a vaccine site with a potent recall antigen such as tetanus/diphtheria (Td) toxoid can significantly improve the lymph node homing and efficacy of tumor antigen-specific DC vaccines. Patients given Td had enhanced DC migration bilaterally and significantly improved survival. In mice, Td pre-conditioning also enhanced bilateral DC migration and suppressed tumor growth in a manner dependent on the chemokines CCL3 and CCL21 and Td-activated CD4.sup.+ T cells. Interference with any component of this axis markedly reduced Td-mediated DC migration and antitumor responses. Our clinical studies and corroborating investigations in mice suggest that pre-conditioning with a potent recall antigen represents a viable strategy to increase DC homing to lymph nodes and improve antitumor immunotherapy.