In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[Q]: Current hemagglutinin (HA)-based seasonal influenza vaccines induce vaccine strain-specific neutralizing antibodies that usually fail to provide protection against mismatched circulating viruses. Inclusion in the vaccine of highly conserved internal proteins such as the nucleoprotein (NP) and the matrix protein 1 (M1) was shown previously to increase vaccine efficacy by eliciting cross-reactive T-cells. However, appropriate delivery systems are required for efficient priming of T-cell responses. In this study, we demonstrated that administration of novel self-amplifying mRNA (SAM 1 ) vectors expressing influenza NP (SAM (NP)), M1 (SAM(M1)), and NP and M1 (SAM(M1-NP)) delivered with lipid nanoparticles (LNP) induced robust polyfunctional CD4 T helper 1 cells, while NP-containing SAM also induced cytotoxic CD8 T cells. Robust expansions of central memory (T CM ) and effector memory (T EM ) CD4 and CD8 T cells were also measured. An enhanced recruitment of NPspecific cytotoxic CD8 T cells was observed in the lungs of SAM(NP)-immunized mice after influenza infection that paralleled with reduced lung viral titers and pathology, and increased survival after homologous and heterosubtypic influenza challenge. Finally, we demonstrated for the first time that the co-administration of RNA (SAM(M1-NP)) and protein (monovalent inactivated influenza vaccine (MIIV)) was feasible, induced simultaneously NP-, M1-and HA-specific T cells and HA-specific neutralizing antibodies, and enhanced MIIV efficacy against a heterologous challenge. In conclusion, systemic administration of SAM vectors expressing conserved internal influenza antigens induced protective immune responses in mice, supporting the SAM 1 platform as another promising strategy for the development of broad-spectrum universal influenza vaccines.
[A]: Self-Amplifying mRNA Vaccines Expressing Multiple Conserved Influenza Antigens Confer Protection against Homologous and Heterosubtypic Viral Challenge

[Q]: Keywords: interferon, interferon-stimulated genes, tumor necrosis factor-related apoptosis-inducing ligand, acute lung injury, innate immunity, influenza, respiratory syncytial virus, coronavirus FiGURe 1 | PRRs and their downstream signaling pathways in virus-induced iFN induction. In viral infection, type I IFNs are induced by TLR, RLR, CLR, and cytosolic nucleic acid sensors. Cell membrane-located TLRs ligate to viral envelope proteins (e.g., TLR2/herpes simplex virus), upon which they recruit MyD88. MyD88 interacts with IRAK kinase (IRAK-1, -2, or -4) that either directly activate IRF1 or interact with TRAF6, which induces IRF7 or assembles with TAK1. TAK1 forms a complex with TAB-1/-2 and -3 and subsequently either activates the MAPK kinases p38 and JNK, leading to AP-1 phosphorylation and nuclear translocation, or induces ubiquitination of NEMO followed by IB degradation and NFB activation. Endosomal TLRs recognizing viral nucleic acid and signal via the adaptor protein MyD88 (for TLR7/8/9) or interact with TRIF (for TLR3) followed by TRAF3, TANK, and TBK1 activation. TBK1 and IKK then phosphorylate and activate IRF3 and IRF7. Additionally, TRIF can interact with TRAF6 to initiate TAK1 signaling. Both RLRs, RIG-I and MDA-5, recognize nucleic acid contents in the cytoplasm and stimulate the mitochondrial anchored IPS-1 for dimerization followed by TRADD recruitment that acts via TRAF3 on IRF3 and IRF7. Additionally, IPS-1 can interact with FADD and RIP1 to activate NFB via IKK activated by caspase-8 and -10. Also PKR signaling results in NFB activation and nuclear translocation. The dsDNA sensor cGAS produces cGAMP that activates ER-located STING that via TBK1 induces IRF3 translocation and type I IFN production. CLRs play a minor role in viral recognition; however, DC-SIGN activates the small GTPase Ras and Raf protein kinase, followed by NFB activation. Type III IFN are induced by TLR3, TLR9, and via RIG-I and peroxisomal-resident IPS-1. Especially IRF1, but also NFB, IRF3, and IRF7 are implicated in IFN- production, with the latter being stabilized by Med23.
[A]: The impact of the interferon/TNF- Related Apoptosis-inducing Ligand Signaling Axis on Disease Progression in Respiratory viral infection and Beyond

[Q]: A high proportion of dogs suffer from respiratory disease when they are placed in kennels for vacation or re-homing. The role of Mycoplasma cynos as an initiating agent in canine infectious respiratory disease was investigated by examining the serological response of dogs to this organism at the time of entry into a large re-homing kennel. Forty-two paired serum samples from dogs (21-day interval) were examined for antibody to M. cynos using Western blotting. The development of antibody in the serum was related to clinical disease recorded over the same period. Sixty seven per cent of the dogs showed a two-fold or greater rise in antibody to M. cynos during the first 3 weeks in the kennel. Reactivity with a 45 kDa antigen was dominant. Of those showing a positive serological reaction, 80% had recorded clinical respiratory disease while 20% remained healthy. The findings of this study show that an antibody response to M. cynos is common in dogs entering the re-homing kennel and is positively related to the development of clinical respiratory disease. #
[A]:
Serological evidence of Mycoplasma cynos infection in canine infectious respiratory disease